Alzheimer's disease (AD) is a cognitive disease with high morbidity and mortality. In AD patients, the diversity of the gut microbiota is altered, which influences pathology through the gut-brain axis. Probiotic therapy alleviates pathological and psychological consequences by restoring the diversity of the gut microbial flora. This study addresses the role of altered gut microbiota in the progression of neuroinflammation, which is a major hallmark of AD. This process begins with the activation of glial cells, leading to the release of proinflammatory cytokines and the modulation of cholinergic anti-inflammatory pathways. Short-chain fatty acids, which are bacterial metabolites, provide neuroprotective effects and maintain blood‒brain barrier integrity. Furthermore, the gut microbiota stimulates oxidative stress and mitochondrial dysfunction, which promote AD progression. The signaling pathways involved in gut dysbiosis-mediated neuroinflammation-mediated promotion of AD include cGAS-STING, C/EBPβ/AEP, RAGE, TLR4 Myd88, and the NLRP3 inflammasome. Preclinical studies have shown that natural extracts such as Ganmaidazao extract, isoorentin, camelia oil, Sparassis crispa-1, and xanthocerasides improve gut health and can delay the worsening of AD. Clinical studies using probiotics such as Bifidobacterium spp., yeast beta-glucan, and drugs such as sodium oligomannate and rifaximine have shown improvements in gut health, resulting in the amelioration of AD symptoms. This study incorporates the most current research on the pathophysiology of AD involving the gut microbiota and highlights the knowledge gaps that need to be filled to develop potent therapeutics against AD.

Oxidative stress, dysbiosis, and immune dysregulation have been confirmed to play pivotal roles in the complex pathogenesis of inflammatory bowel disease (IBD). Herein, we design copper ion-luteolin nanocomplexes (CuL NCs) through a metal-polyphenol coordination strategy, which plays a multifaceted role in the amelioration of IBD. The fabricated CuL NCs function as therapeutic agents with exceptional antioxidant and anti-inflammatory capabilities because of their great stability and capacity to scavenge reactive oxygen species (ROS). It can effectively modulate the inflammatory microenvironment including facilitating the efficient reduction of pro-inflammatory cytokine levels, protecting intestinal epithelial cells, promoting mucosal barrier repair and regulating intestinal microbiota. In addition, CuL NCs have been found to enhance cellular antioxidant and anti-inflammatory capacities by regulating the nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) oxidative stress pathway and nuclear factor kappa B (NF-κB) signaling pathway, respectively. Notably, CuL NCs demonstrate significant prophylactic and therapeutic efficacy in mouse models with typical IBD, including ulcerative colitis (UC) and Crohn's disease (CD). This study provides a new approach for building multifaceted therapeutic platforms for natural products to treat IBD.

The aim of study was to investigate the effects of dark environment on production performance, intestinal barrier function and clock-related gene expression in rabbits. Forty weaned rabbits with similar body weight (35-day-old) were randomly divided into 2 treatments (20 replicates per treatment, 1 rabbit per replicate: normal light group (12 L and 12 D) or total dark group (24 D). The experimental period lasted for 10 days, with an adaptation period of 3 days and a subsequent formal experimental period of 7 days. The results showed that feed-to-weight ratio of rabbits in total dark group was significantly decreased compared with normal light group. Dark treatment significantly increased gene expression of claudin-1, mucin1 in duodenum, occludin-1, claudin-1, zona occludens 1 (ZO1), junctional adhesion molecule 2 (JAM2) and interleukin 10 (IL10) in jejunum, claudin-1, mucin1, ZO1 and IL10 in ileum and clock, melatonin 1 A, melatonin 1B, and period1 in cecum compared with normal light group. Total dark treatment increased alpha diversity via increasing chao1 index, observed species index and faith_pd index of cecal flora. Total dark treatment significantly reduced percentage of Deferobacterium at phylum level in cecum, but significantly increased percentage of Rumenococci at genus level. There is an insignificant increasing tendency of acetic acid and propionic acid content of soft feces in total dark group. In conclusion, total dark treatment improves feed conversion efficiency in rabbits and activates cecum clock system, which increased diversity of bacterial flora and production of short-chain fatty acids, then increases intestinal barrier function.

Exploring the associations between microbes and drugs offers valuable insights into their underlying mechanisms. Traditional wet lab experiments, while reliable, are often time-consuming and labor-intensive, making computational approaches an attractive alternative. Existing similarity-based machine learning models for predicting microbe-drug associations typically rely on integrated similarities as input, neglecting the unique contributions of individual similarities, which can compromise predictive accuracy. To overcome these limitations, we develop MPEMDA, a novel method that pre-completes the microbe-drug association matrix using various similarity combinations and employs a label propagation algorithm with error correction to predict microbe-drug associations. Compared with existing methods, MPEMDA simultaneously utilizes the integrated and individual similarities obtained through the Similarity Network Fusion (SNF) method to pre-complete the known drug-microbe association matrix, followed by error correction to optimize the predictive scores generated by the label propagation algorithm. Experimental results on three benchmark datasets show that MPEMDA outperforms state-of-the-art methods in both the 5-fold cross-validation and de novo test. Additionally, case studies on drugs and microbes highlight the method's strong potential to identify novel microbe-drug associations. The MPEMDA code is available at https://github.com/lyx8527/MPEMDA.

Research on fecal microbiota changes during hospitalization of horses with colic is emerging.

Describe changes of the fecal microbiota during hospitalization of horses with colic caused by inflammatory (INFL), simple (SIMPLE), and strangulated (STR) obstructions, and investigate associations with survival.

Twenty-three horses with colic: 9 in INFL, 5 in STR, and 9 in SIMPLE groups. Seventeen horses survived, and 6 were euthanized.

Prospective observational study. Fecal samples were collected on admission (D1), on days 3 (D3) and 5 (D5). Bacterial taxonomy profiling was obtained by V1V3 16S amplicon sequencing. Data were compared using a 2-way permutational analysis of variance (PERMANOVA). Linear discriminant analysis Effect Size (LEfSE) analysis identified significant bacterial population differences, with significance set at p < 0.05 and a linear discriminant analysis (LDA) cut-off > 3.0.

Alpha diversity indices remained stable during hospitalization within each colic group. However, at D5, the INFL group had significantly higher richness (p < 0.01) and diversity (Shannon, p < 0.001 and Simpson, p < 0.05) than other colic types. Beta diversity (Jaccard membership and Bray-Curtis indices) was significantly different in the INFL compared to SIMPLE and STR groups (both p < 0.001) but not between SIMPLE and STR. Beta diversity membership analysis by analysis of molecular variance (AMOVA) indicated a significant difference between survivors and non-survivors within the INFL group (p < 0.01). Increased relative abundances of Bacilliculturomica and Saccharofermentans were associated with survival.

Microbiota showed no significant variation over 5 days of hospitalization. Colic type influenced fecal microbiota more than hospitalization duration. Specific bacterial populations may differ between survival and non-survival groups.

Helicobacter pylori is an extremely common cause of gastritis that can lead to gastric adenocarcinoma over time. Approximately half of the world's population is infected with H. pylori, making gastric cancer the fourth leading cause of cancer-related deaths worldwide. Innate immunity significantly contributes to systemic and local immune responses, maintains homeostasis, and serves as the vital link to adaptive immunity, and in doing so, mediates H. pylori infection outcomes and consequent cancer risk and development. The gastric innate immune system, composed of gastric epithelial and myeloid cells, is uniquely challenged by its need to interact simultaneously and precisely with commensal microbiota, exogenous pathogens, ingested substances, and endogenous exfoliated cells. Additionally, innate immunity can be detrimental by promoting chronic infection and fibrosis, creating an environment conducive to tumor development. This review summarizes and discusses the complex role of innate immunity in H. pylori infection and subsequent gastric oncogenesis, and in doing so, provides insights into how these pathways can be exploited to improve prevention and treatment.

Although the benefits of low-germ diets for patients are increasingly being questioned, their application in practice is widespread. The aim of this review is to summarise the current data and evaluate the effectiveness of the neutropenic diet (ND) in adult haemato-oncological patients to provide a basis for practical guidelines.

A systematic search was conducted in four electronic databases (Medline (Ovid), CINAHL (EBSCO), EMBASE (Ovid) and Cochrane CENTRAL) to identify English and German randomised controlled trials (RCTs) concerning the effectiveness of an ND in adult haematological patients. The main endpoints were fever and systemic infections, gastrointestinal (GI) infections, mortality, nutritional status and hospitalisation length.

A total of five RCTs with 510 adult patients were included in this systematic review. All patients received high-dose chemotherapy in order to treat haemato-oncological malignancies. None of the analysed endpoints showed a significant advantage of the ND compared to the control group.

An ND does not have a beneficial effect on infection rates, GI health, mortality or hospitalisation length for haemato-oncological patients. On the contrary, an ND tends to negatively affect the patient's nutritional status; therefore, an adaption in clinical routine should take place.

Multiple sclerosis (MS) is defined as an inflammatory disorder that chronically affects the central nervous system of young people mostly and is distributed globally. It is associated with degeneration and demyelination of the myelin sheath around the nerves, resulting in multiple neurological disability symptoms ranging from mild to severe cases that end with paralysis sometimes. MS is one of the rising diseases globally that is unfortunately associated with reduced quality of life and adding national economic burdens. The definite MS mechanism is not clearly defined; however, all the previous researches confirm the role of the immune system as the master contributor in the pathogenesis. Innate and adaptive immune cells are activated peripherally then attracted toward the central nervous system (CNS) due to the breakdown of the blood-brain barrier. Recently, the gut-brain axis was shown to depend on gut metabolites that are produced by different microorganisms in the colon. The difference in microbiota composition between individuals is responsible for diversity in secreted metabolites that affect immune responses locally in the gut or systemically when reach blood circulation to the brain. It may enhance or suppress immune responses in the central nervous system (CNS) (repeated short forms); consequently, it may exacerbate or ameliorate MS symptoms. Recent data showed that some metabolites can be used as adjuvant therapy in MS and other inflammatory diseases. This review sheds light on the nature of MS and the possible interaction between gut microbiota and immune system regulation through the gut-brain axis, hence contributing to MS pathogenesis.

An increasing number of studies have revealed that gut microbiota influences the development and progression of Colorectal cancer (CRC). However, whether a causal relationship exists between the two remains unclear, and the role of immune cells in this context is not well understood.

To elucidate the causal relationship between gut microbiota and CRC and to explore the potential mediating role of circulating immune cells.

To analyze the causal relationship between gut microbiota and CRC, we employed a univariable Mendelian randomization (UVMR) approach. Subsequently, a two-step multivariable Mendelian randomization (MVMR) to assess the potential mediating role of circulating immune cells. Primarily, applied the Inverse-Variance Weighted method to evaluate the causal relationship between exposure and outcome. To ensure the robustness of the results linking gut microbiota and CRC, we validated the findings using Robust Inverse-Variance Weighted, Penalized Inverse-Variance Weighted, and Penalized Robust Inverse-Variance Weighted methods. Additionally, we employed MR-Egger Intercept to mitigate the influence of horizontal pleiotropy. MR-PRESSO was used to detect and correct outliers by excluding anomalous instrumental variables. Finally, we supplemented our analysis with methods such as Bayesian Weighted Mendelian Randomization (BWMR), Maximum-Likelihood, Lasso, Debiased Inverse Variance Weighted, and Contamination Mixture to establish a robust and compelling causal relationship.

After accounting for reverse causality, horizontal pleiotropy, and various methodological corrections, Bifidobacterium kashiwanohense, GCA-900066755 sp900066755, Geminocystis, and Saccharofermentanaceae exhibited strong and robust causal effects on CRC. Specifically, CD40 on monocytes (2.82%) and CD45 on CD33+HLA-DR+CD14- cells (12.87%) mediated the causal relationship between Bifidobacterium kashiwanohense and CRC risk. Furthermore, CD45 on CD33-HLA-DR+ (3.94%) mediated the causal relationship between GCA-900066755 sp900066755 and CRC risk. Additionally, terminally differentiated CD4+T cells (11.55%) mediated the causal relationship between Geminocystis and CRC risk. Lastly, CD40 on monocytes (2.35%), central memory CD4+T cells (5.76%), and CD28 on CD28+CD45RA+CD8+T cells (5.00%) mediated the causal relationship between Saccharofermentanaceae and CRC risk.

Our mediation MR analysis provides genetic evidence suggesting that circulating immune cells may mediate the causal relationship between gut microbiota and CRC. The identified associations and mediation effects offer new insights into potential therapeutic avenues for CRC.

Irritable bowel syndrome (IBS) is a prevalent gastrointestinal disorder characterized by chronic abdominal pain, bloating, and altered bowel habits. Low-FODMAP diets, which involve restricting fermentable oligosaccharides, disaccharides, monosaccharides, and polyols, have emerged as an effective dietary intervention for alleviating IBS symptoms. This review paper aims to synthesize current insights into the impact of a low-FODMAP diet on the gut microbiome and its mechanisms of action in managing IBS. We explore the alterations in microbial composition and function associated with a low-FODMAP diet and discuss the implications of these changes for gut health and symptom relief. Additionally, we examine the balance between symptom improvement and potential negative effects on microbial diversity and long-term gut health. Emerging evidence suggests that while a low-FODMAP diet can significantly reduce IBS symptoms, it may also lead to reductions in beneficial microbial populations. Strategies to mitigate these effects, such as the reintroduction phase and the use of probiotics, are evaluated. This review highlights the importance of a personalized approach to dietary management in IBS, considering individual variations in microbiome responses. Understanding the intricate relationship between diet, the gut microbiome, and IBS symptomatology will guide the development of more effective, sustainable dietary strategies for IBS patients.

Prebiotics are substrates selectively utilized by microorganisms to confer health benefits to their hosts. Various prebiotics have been supplemented in standard milk formulas for infants who cannot be exclusively breastfed, aiming to provide benefits similar to those of breast milk. One of the most commonly used prebiotics is a mixture of 90% short-chain galacto-oligosaccharides and 10% long-chain fructo-oligosaccharides (scGOS/lcFOS [9:1]). Systematic review and meta-analysis were conducted to determine the effectiveness of scGOS:lcFOS (9:1) supplementation in standard milk formula for improving gastrointestinal health and immunity among healthy infants and toddlers, using parameters such as stool pH and intestinal colonization with beneficial bacteria. This systematic review was prepared in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines. Randomized clinical trials comparing scGOS/lcFOS (9:1)-supplemented formula versus placebo- or non-supplemented formula milk were eligible for inclusion. Related studies on gastrointestinal health and immunity among healthy infants up to five years old were searched from the earliest available date until February 29, 2024. Eighteen publications (number of participants=1,675) were selected for the systematic review, of which 11 were subsequently subjected to a meta-analysis. Results showed that the standard formula supplemented with scGOS/lcFOS (9:1) was well tolerated and conferred various gastrointestinal health and immunity to healthy infants and toddlers. These findings support the supplementation of standard milk formula with scGOS/lcFOS (9:1) for healthy infants and toddlers.

The intestinal microbiota plays a crucial role in health and disease. This study aimed to assess the composition and functional diversity of the intestinal microbiota in donkeys and cows by examining samples collected from different segments of the digestive tract using two distinct techniques: direct swab sampling and faecal sampling.

In this study, we investigated and compared the effects of multiple factors on the composition and function of the intestinal microbial community. Approximately 300 GB of metagenomic sequencing data from 91 samples obtained from various segments of the digestive tract were used, including swabs and faecal samples from monogastric animals (donkeys) and polygastric animals (cows). We assembled 4,004,115 contigs for cows and 2,938,653 contigs for donkeys, with a total of 9,060,744 genes. Our analysis revealed that, compared with faecal samples, swab samples presented a greater abundance of Bacteroidetes, whereas faecal samples presented a greater abundance of Firmicutes. Additionally, we observed significant variations in microbial composition among different digestive tract segments in both animals. Our study identified key bacterial species and pathways via different methods and provided evidence that multiple factors can influence the microbial composition. These findings provide new insights for the accurate characterization of the composition and function of the gut microbiota in microbiome research.

The results obtained by both sampling methods in the present study revealed that the composition and function of the intestinal microbiota in donkeys and cows exhibit species-specific and region-specific differences. These findings highlight the importance of using standardized sampling protocols to ensure accurate and consistent characterization of the intestinal microbiota in various animal species. The implications and underlying mechanisms of these associations provide multiple perspectives for future microbiome research.

The human gastrointestinal microbiota plays a vital role in maintaining host health and preventing diseases, prompting the creation of simulators to replicate this intricate system. The Simulator of the Human Intestinal Microbial Ecosystem (SHIME®), a multicompartment dynamic simulator, has emerged as a pivotal in vitro model for studying the interactions and interferences within the human gut microbiota. The continuous and real-time monitoring hallmarks, along with the programmatically flexible setup, bestow SHIME® with the ability to mimic the entire human intestinal ecosystem with high dynamics and stability, allowing the evaluation of various treatments on the bowel microbiota in a controlled environment. This review outlines recent developments in SHIME® systems, including the M-SHIME®, Twin-SHIME®, Triple-SHIME®, and Toddle SHIME® models, highlighting their applications in the fields of food and nutritional science, drug development, gut health research, and traditional Chinese medicine. Additionally, the prospect of SHIME® integrating with other advanced technologies is also discussed. The findings underscore the versatility of SHIME® technology, demonstrating its significant contributions to current gut ecosystem research and its potential for future innovation in microbiome-related fields.

Non-Alcoholic Fatty Liver Disease (NAFLD) affects approximately 32.4% of the global population and poses a significant health concern. Emerging evidence underscores the pivotal role of the gut microbiota-including bacteria, viruses, fungi, and parasites-in the development and progression of NAFLD. Dysbiosis among gut bacteria alters key biological pathways that contribute to liver fat accumulation and inflammation. The gut virome, comprising bacteriophages and eukaryotic viruses, significantly shapes microbial community dynamics and impacts host metabolism through complex interactions. Similarly, gut fungi maintain a symbiotic relationship with bacteria; the relationship between gut fungi and bacteria is crucial for overall host health, with certain fungal species such as Candida in NAFLD patients showing detrimental associations with metabolic markers and liver function. Additionally, the "hygiene hypothesis" suggests that reduced exposure to gut parasites may affect immune regulation and metabolic processes, potentially influencing conditions like obesity and insulin resistance. This review synthesizes current knowledge on the intricate interactions within the gut microbiota and their associations with NAFLD. We highlight the therapeutic potential of targeting these microbial communities through interventions such as probiotics, prebiotics, and fecal microbiota transplantation. Addressing the complexities of NAFLD requires comprehensive strategies that consider the multifaceted roles of gut microorganisms in disease pathology.

The ameliorating effects and mechanisms of Morchella esculenta polysaccharides (MEP-1) on lipid metabolism were investigated in high-fat diet (HFD) mice. The results showed that MEP-1 intervention significantly reduced serum TC, TG, LDL-C, and inflammatory factors (TNF-α, IL-1β and IL-6) in HFD mice in a dose-dependent manner, and high-dose (400 mg/kg/d) exhibited the most significant reductive effects. In addition, MEP-1 significantly recovered the gut microbiota disorders caused by HFD, especially decreasing the ratio of Firmicutes and Bacteroidetes (F/B) and increasing the dominant bacterial of Muribaculaceae_genus, Bacteroides, Alistipes and Enterococcus. Moreover, MEP-1 promoted the production of SCFAs and increased the expression levels of Occludin, Claudin and Muc2, also regulated lipid metabolism disorder and inflammation by inhibiting TLR4/MyD88/NF-κB via the gut-liver axis. In addition, serum metabolomic analysis revealed that l-phenylalanine, l-arginine and acetylcholine were significantly upregulated with MEP-1 intervention, and were negatively correlated with blood lipid level, in which l-arginine could activate NO/PPARα/CPT1A pathway to ameliorate lipid metabolism disorders. Such results demonstrated that gut microbiota, amino acid metabolic and insulin secretion pathways might be the important factors that mediated the regulation of MEP-1 in lipid metabolism. The results also provided new evidence and strategies for the application of MEP-1 as functional foods.

The gut microbiome has a well-documented relationship with host fitness, physiology, and behavior. However, most of what is known comes from captive animals where diets and environments are more homogeneous or controlled. Studies in wild populations that experience dynamic environments and have natural life history variation are less common but are key to understanding the drivers of variation in the gut microbiome. Here we examine a wild population of yellow-bellied marmots (Marmota flaviventer), an obligate winter hibernator, to quantify multivariate associations between host-associated factors (e.g., age, sex, environmental harshness, and social behavior) and gut microbial composition. Across 5 years and 143 individuals, we found that males had a higher relative abundance of microbes associated with mass gain and cellulose digestion, which suggests a metabolic investment in mass gain (such as phylum Firmicutes and family Lachnospiraceae). By contrast, females had higher relative abundances of microbes associated with inflammation and metabolism (from microbial groups such as Tenericutes and Ruminococcus), possibly reflecting the importance of lactation and offspring investment. Post hoc analyses of lactating females showed a negative relationship with the abundance of microbes associated with mass gain but a positive relationship with microbes associated with metabolic energy, suggesting a trade-off between investment in pups and maternal mass gain. Older animals also had reduced Proteobacteria relative abundance, a phylum associated with reduced inflammation. Results demonstrate that sex and age-based traits, not sociality or environmental harshness, are associated with microbe-mediated metabolism and inflammation in a wild, hibernating mammal.

Several perinatal factors influence the intestinal microbiome of newborns during the first days of life, whether during delivery or even in utero. These factors may increase the risk of developing necrotizing enterocolitis (NEC) by causing dysbiosis linked to a NEC-associated microbiota, which may also be associated with other gastrointestinal problems. The objective of our study was to evaluate the potential risks associated with microbial shifts in newborns with gastrointestinal symptoms and identify the intestinal microbiota of neonates at risk for NEC.During the study period, 310 preterm and term newborns' first passed meconium occurring within 72 h of birth were collected, and the microbiome was analyzed. We identified the risk factors in the NEC/FI group. Regarding microbiota, we compared the bacterial abundance between the NEC/FI group at the phylum and genus levels and explored the differences in the microbial composition of the 1st stool samples. A total of 14.8% (n = 46) of the infants were diagnosed with NEC or FI. In univariate analysis, the mean gestational age and birth weight were significantly lower in the NEC/FI group (p < 0.001). Prolonged rupture of membranes (PROM) > 18 h, chorioamnionitis, and histology were significantly higher in the NEC/FI group (p < 0.001). Multivariate analysis showed that gestational age (GA), prolonged membrane rupture (> 18 h), and early onset sepsis were consistently associated with an increased risk of NEC/FI. Infants diagnosed with NEC/FI exhibited a significantly lower abundance of Actinobacteria at the phylum level than the control group (p < 0.001). At the genus level, a significantly lower abundance of Streptococcus and Bifidobacterium which belong to the Actinobacteria phylum, was observed in the NEC/FI group (p < 0.001). Furthermore, the NEC/FI had significantly lower alpha diversities (Shannon Index,3.39 vs. 3.12; P = 0.044, respectively). Our study revealed that newborns with lower diversity and dysbiosis in their initial gut microbiota had an increased risk of developing NEC, with microbiota differences appearing to be associated with NEC/FI. Dysbiosis could potentially serve as a predictive marker for NEC- or GI-related symptoms.

Animal gut microbiomes are critical to host physiology and fitness. The gut microbiomes of fishes-the most abundant and diverse vertebrate clade-have received little attention relative to other clades. Coral reef fishes, in particular, make up a wide range of evolutionary histories and feeding ecologies that are likely associated with gut microbiome diversity. The repeated evolution of herbivory in fishes and mammals also allows us to examine microbiome similarity in relationship to diet across the entire vertebrate tree of life. Here, we generate a large coral reef fish gut microbiome dataset (n = 499 samples, 19 species) and combine it with a diverse aggregation of public microbiome data (n = 447) to show that host diet drives significant convergence between coral reef fish and mammalian gut microbiomes. We demonstrate that this similarity is largely driven by carnivory and herbivory and that herbivorous and carnivorous hosts exhibit distinct microbial compositions across fish and mammals. We also show that fish and mammal gut microbiomes share prominent microbial taxa, including Ruminoccocus spp. and Akkermansia spp., and predicted metabolic pathways. Despite the major evolutionary and ecological differences between fishes and mammals, our results reveal that their gut microbiomes undergo similar dietary selective pressures. Thus, diet, in addition to phylosymbiosis must be considered even when comparing the gut microbiomes of distantly related hosts.

The human microbiome is a complex and dynamic system that plays important roles in human health and disease. However, there remain limitations and theoretical gaps in our current understanding of the intricate relationship between microbes and humans. In this narrative review, we integrate the knowledge and insights from various fields, including anatomy, physiology, immunology, histology, genetics, and evolution, to propose a systematic framework. It introduces key concepts such as the 'innate and adaptive genomes', which enhance genetic and evolutionary comprehension of the human genome. The 'germ-free syndrome' challenges the traditional 'microbes as pathogens' view, advocating for the necessity of microbes for health. The 'slave tissue' concept underscores the symbiotic intricacies between human tissues and their microbial counterparts, highlighting the dynamic health implications of microbial interactions. 'Acquired microbial immunity' positions the microbiome as an adjunct to human immune systems, providing a rationale for probiotic therapies and prudent antibiotic use. The 'homeostatic reprogramming hypothesis' integrates the microbiome into the internal environment theory, potentially explaining the change in homeostatic indicators post-industrialization. The 'cell-microbe co-ecology model' elucidates the symbiotic regulation affecting cellular balance, while the 'meta-host model' broadens the host definition to include symbiotic microbes. The 'health-illness conversion model' encapsulates the innate and adaptive genomes' interplay and dysbiosis patterns. The aim here is to provide a more focused and coherent understanding of microbiome and highlight future research avenues that could lead to a more effective and efficient healthcare system.

SUMMARYThe human intestinal tract harbors a profound variety of microorganisms that live in symbiosis with the host and each other. It is a complex and highly dynamic environment whose homeostasis directly relates to human health. Dysbiosis of the gut microbiota and polymicrobial biofilms have been associated with gastrointestinal diseases, including irritable bowel syndrome, inflammatory bowel diseases, and colorectal cancers. This review covers the molecular composition and organization of intestinal biofilms, mechanistic aspects of biofilm signaling networks for bacterial communication and behavior, and synergistic effects in polymicrobial biofilms. It further describes the clinical relevance and diseases associated with gut biofilms, the role of biofilms in antimicrobial resistance, and the intestinal host defense system and therapeutic strategies counteracting biofilms. Taken together, this review summarizes the latest knowledge and research on intestinal biofilms and their role in gut disorders and provides directions toward the development of biofilm-specific treatments.

Beyond the pivotal roles of the gut microbiome in initiating physiological processes and modulating genetic factors, a query persists: Can a single gene mutation alter the abundance of the gut microbiome community? Not only this, but the intricate impact of gut microbiome composition on skin pigmentation has been largely unexplored.

Based on these premises, our study examines the abundance of lipase-producing gut microbes about differential gene expression associated with bile acid synthesis and lipid metabolism-related blood metabolites in red (whole wild) and white (whole white wild and SCARB1-/- mutant) Oujiang colour common carp. Following the disruption of the SCARB1 gene in the resulting mutant fish with white body colour (SCARB1-/-), there is a notable decrease in the abundance of gut microbiomes (Bacillus, Staphylococcus, Pseudomonas, and Serratia) associated with lipase production. This reduction parallels the downregulation seen in wild-type white body colour fish (WW), as contrasting to the wild-type red body colour fish (WR). Meanwhile, in SCARB1-/- fish, there was a downregulation noted not only at the genetic and metabolic levels but also a decrease in lipase-producing bacteria. This consistency with WW contrasts significantly with WR. Similarly, genes involved in the bile acid synthesis pathway, along with blood metabolites related to lipid metabolism, exhibited downregulation in SCARB1-/- fish.

The SCARB1 knockout gene blockage led to significant alterations in the gut microbiome, potentially influencing the observed reduction in carotenoid-associated skin pigmentation. Our study emphasizes that skin pigmentation is not only impacted by genetic factors but also by the gut microbiome. Meanwhile, the gut microbiome's adaptability can be rapidly shaped and may be driven by specific single-gene variations.

The intestinal microbiota represents a key element in maintaining the homeostasis and health conditions of the host. Vascular pathologies and other risk factors such as aging have been recently associated with dysbiosis. The qualitative and quantitative alteration of the intestinal microbiota hinders correct metabolic homeostasis, causing structural and functional changes of the intestinal wall itself. Impairment of the intestinal microbiota, combined with the reduction of the barrier function, worsen the pathological scenarios of peripheral tissues over time, including the vascular one. Several experimental evidence, collected in this review, describes in detail the changes of the intestinal microbiota in dysbiosis associated with vascular alterations, such as atherosclerosis, hypertension, and endothelial dysfunction, the resulting metabolic disorders and how these can impact on vascular health. In this context, the gut-vascular axis is considered, for the first time, as a merged unit involved in the development and progression of vascular pathologies and as a promising target. Current approaches for the management of dysbiosis such as probiotics, prebiotics and dietary modifications act mainly on the intestinal district. Postbiotics, described as preparation of inanimate microorganisms and/or their components that confers health benefits on the host, represent an innovative strategy for a dual management of intestinal dysbiosis and vascular pathologies. In this context, this review has the further purpose of defining the positive effects of the supplementation of bacterial strains metabolites (short‑chain fatty acids, exopolysaccharides, lipoteichoic acids, gallic acid, and protocatechuic acid) restoring intestinal homeostasis and acting directly on the vascular district through the gut-vascular axis.

Alzheimer's disease (AD), diabetes mellitus (DM), inflammatory bowel diseases (IBD), and rheumatoid arthritis (RA) are chronic conditions affecting millions globally. Despite differing clinical symptoms, these diseases share pathophysiological mechanisms involving metabolic and immune system dysregulation. This paper examines the intricate connections between these disorders, focusing on shared pathways such as insulin resistance, lipid metabolism dysregulation, oxidative stress, and chronic inflammation. An important aspect is the role of amyloid-beta plaques and tau protein tangles, which are hallmark features of AD. These protein aggregates are influenced by metabolic dysfunction and inflammatory processes similar to those seen in DM, RA, and IBD. This manuscript explores how amyloid and tau pathologies may be exacerbated by shared metabolic and immune dysfunction. Additionally, this work discusses the gut-brain axis and the influence of gut microbiota in mediating disease interactions. Understanding these commonalities opens new avenues for multi-targeted therapeutic approaches that address the root causes rather than merely the symptoms of these conditions. This integrative perspective could lead to more effective interventions and improved patient outcomes, emphasizing the importance of a unified approach in managing these interconnected diseases.

Cirrhosis, a pathological stage that develops from various chronic liver diseases, is characterized by liver fibrosis, pseudolobular formation, and chronic inflammation. When it progresses to the decompensated phase, the mortality rate of cirrhosis can reach 80%. The role of gut microbiota in the progression of liver diseases has received significant attention. Numerous studies have shown that regulating gut microbiota has significant therapeutic effects on preventing and reversing liver cirrhosis. This article reviewed the mechanisms by which gut microbiota influence liver cirrhosis, explaining the effective therapeutic effects of traditional Chinese medicine. Through multi-directional regulation involving signaling pathways, gut microbiota diversity, and restoration of intestinal barrier function, traditional Chinese medicine has been promising in ameliorating liver cirrhosis, providing treatment options and pharmacological guidance for the occurrence and development of liver cirrhosis.

In managed care settings, primates are susceptible to a variety of health complications. A comprehensive understanding of the causes of mortality and their association with management practices is essential for enhancing the welfare of managed care populations such as François' langurs (Trachypithecus francoisi). However, literature addressing prevalent diseases or causes of death in such settings remains limited among François' langurs in managed care. To address this knowledge gap, we conducted an analysis of mortality causes in François' langurs (n = 97) who died of natural causes during a 16-year period (2007-2022) at the Trachypithecus francoisi Rare Animal Breeding Center in Wuzhou, Guangxi, China. Morphological diagnosis and organ system and etiological evaluations were performed. François' langurs were divided into six age-range groups, following previous studies: infant (≤ 1 year old), juvenile (1 to 2 years), sub-adult (2 to 4 years), adult (4 to 10 years), middle-aged (10 to 15 years), and geriatric (> 15 years). Results revealed that the primary causes of mortality in managed care François' langurs were pneumonia (n = 11, 12.22%), neoplasia (n = 7, 7.78%), ileus (n = 7, 7.78%), senility (n = 6, 6.67%), gastroenteritis (n = 6, 6.67%), cardiac disease (n = 5, 5.56%), hemorrhage (n = 5, 5.56%), intestinal adhesion (n = 4, 4.44%), and renal abscess (n = 4, 4.44%). The gastrointestinal system was most frequently implicated in deaths, followed by the respiratory system (n = 17, 18.89%), multisystem disease (n = 16, 17.78%), and cardiovascular system (n = 15, 16.67%). Regarding etiology, infectious or inflammatory (n = 32, 35.56%) and physiological factors (n = 17, 18.89%) were identified as the leading contributors to the high mortality rate. It is imperative for managers to recognize the distinct risk profiles associated with different age groups. Specifically, pneumonia was the principal cause of death in infant and juvenile langurs, while renal disease, neoplasia, gastroenteritis, and intestinal obstruction were the primary causes of death in adult and middle-aged François' langurs and advanced age and cardiac disease were the main causes of death in geriatric langurs.

Insect guts offer unique habitats for microbial colonization, with gut bacteria potentially offering numerous benefits to their hosts. Although Enterococcus has emerged as one of the predominant gut commensal bacteria in insects, its establishment in various niches within the gut has not been characterized well. In this study, Enterococcus mundtii was inoculated into the silkworm (Bombyx mori L.) to investigate its biological functions. Genome-based analysis revealed that its successful colonization is related to adherence genes (ebpA, ebpC, efaA, srtC, and scm). This bacterium did not alter the activities of related metabolic enzymes or the intestinal barrier function. However, significant changes in the gene expressions levels of Att2, CecA, and Lys suggest potential adaptive mechanisms of host immunity to symbiotic E. mundtii. Moreover, 16S metagenomics analysis revealed a significant increase in the relative abundance of E. mundtii in the intestines of silkworms following inoculation. The intestinal microbiome displayed marked heterogeneity, an elevated gut microbiome health index, a reduced microbial dysbiosis index, and low potential pathogenicity in the treatment group. Additionally, E. mundtii enhanced the breakdown of carbohydrates in host intestines. Overall, E. mundtii serves as a beneficial microbe for insects, promoting intestinal homeostasis by providing competitive advantage. This characteristic helps E. mundtii dominate complex microbial environments and remain prevalent across Lepidoptera, likely fostering long-term symbiosis between the both parties. The present study contributes to clarifying the niche of E. mundtii in the intestine of lepidopteran insects and further reveals its potential roles in their insect hosts.

Extensive research has explored the role of gut microbiota in multiple sclerosis (MS). However, the impact of microbial communities in the oral cavity and respiratory tract on MS is an emerging area of investigation.

We aimed to review the current literature related to the nasal, oral, and lung microbiota in people with MS (PwMS).

We conducted a narrative review of clinical and preclinical original studies on PubMed that explored the relationship between the bacterial or viral composition of the nasal, lung, and oral microbiota and MS. Additionally, to find relevant studies not retrieved initially, we also searched for references in related review papers, as well as the references cited within the included studies.

Thirteen studies were meticulously reviewed in three sections; oral microbiota (n = 8), nasal microbiota (n = 3), and lung microbiota (n = 2), highlighting considerable alterations in the oral and respiratory microbiome of PwMS compared to healthy controls (HCs). Genera like Aggregatibacter and Streptococcus were less abundant in the oral microbiota of PwMS compared to HCs, while Staphylococcus, Leptotrichia, Fusobacterium, and Bacteroides showed increased abundance in PwMS. Additionally, the presence of specific bacteria, including Streptococcus sanguinis, within the oral microbiota was suggested to influence Epstein-Barr virus reactivation, a well-established risk factor for MS. Studies related to the nasal microbiome indicated elevated levels of specific Staphylococcus aureus toxins, as well as nasal glial cell infection with human herpes virus (HHV)-6 in PwMS. Emerging research on lung microbiome in animal models demonstrated that manipulating the lung microbiome towards lipopolysaccharide-producing bacteria might suppress MS symptoms. These findings open avenues for potential therapeutic strategies. However, further research is crucial to fully understand the complex interactions between the microbiome and MS. This will help identify the most effective timing, bacterial strains, and modulation techniques.

Nardosinone, a major extract of Rhizoma nardostachyos, plays a vital role in sedation, neural stem cell proliferation, and protection of the heart muscle. However, the huge potential of nardosinone in regulating lipid metabolism and gut microbiota has not been reported, and its potential mechanism has not been studied.

To explore the regulation of nardosinone on liver lipid metabolism and gut microbiota.

In this study, the role of nardosinone in lipid metabolism was investigated in vitro and in vivo by adding it to mouse feed and HepG2 cell culture medium. And 16S rRNA gene sequencing was used to explore its regulatory effect on gut microbiota.

Results showed that nardosinone could improve HFD-induced liver injury and abnormal lipid metabolism by promoting mitochondrial energy metabolism in hepatocytes, alleviating oxidative stress damage, and regulating the composition of the gut microbiota. Mechanistically, combined with network pharmacology and reverse docking analysis, it was predicted that CYP2D6 was the target of nardosinone, and the binding was verified by cellular thermal shift assay (CETSA).

This study highlights a novel mechanism function of nardosinone in regulating lipid metabolism and gut microbiota. It also predicts and validates CYP2D6 as a previously unknown regulatory target, which provides new possibilities for the application of nardosinone and the treatment of metabolic-associated fatty liver disease.

Guillain-Barré Syndrome (GBS) is an autoimmune disease that typically develops after a previous gastrointestinal (GI) infection. However, the exact association between Gut Microbiota (GM) and GBS still remains unknown due to various challenges. This study aimed to investigate the potential causal association between GM and GBS by using a two-sample Mendelian Randomization (TSMR) analysis.

Utilizing the largest available genome-wide association study (GWAS) meta-analysis from the MiBioGen consortium (n = 13,266) as a foundation, we conducted a TSMR to decipher the causal relationship between GM and GBS. Various analytical methods were employed, including the inverse variance weighted (IVW), MR-PRESSO, MR-Egger, and weighted median. The heterogeneity of instrumental variables (IVs) was assessed using Cochran's Q statistics.

The analysis identified three microbial taxa with a significantly increased risk association for GBS, including Ruminococcus gnavus group (OR = 1.40, 95 % CI: 1.07-1.83), Ruminococcus gauvreauii group (OR = 1.51, 95 % CI: 1.02-2.25), and Ruminococcaceae UCG009 (OR = 1.42, 95 % CI: 1.02-1.97), while Eubacterium brachy group (OR = 1.44, 95 % CI: 1.10-1.87) and Romboutsia (OR = 1.67, 95 % CI: 1.12-2.47) showed a suggestively causal association. On the other hand, Ruminococcaceae UCG004 (OR = 0.61, 95 % CI: 0.41-0.91) had a protective effect on GBS, while Bacilli (OR = 0.60, 95 % CI: 0.38-0.96), Gamma proteobacteria (OR = 0.63, 95 % CI: 0.41-0.98) and Lachnospiraceae UCG001 (OR = 0.69, 95 % CI: 0.49-0.96) showed a suggestively protective association for GBS.

The MR analysis suggests a potential causal relationship between specific GM taxa and the risk of GBS. However, further extensive research involving diversified populations is imperative to validate these findings.

Studies have indicated a close association between dysbiosis of the gut microbiota and chronic sinusitis. However, the causal relationship between the gut microbiota and the risk of chronic sinusitis remains unclear.

Using genome-wide association study (GWAS) data for the gut microbiota and chronic sinusitis, we conducted a two-sample Mendelian randomization (MR) study to determine the potential causal relationship between the microbiota and chronic sinusitis. We employed the inverse variance-weighted (IVW) method as the primary analytical approach to estimate the effect. Additionally, sensitivity, heterogeneity, and pleiotropy analyses were conducted to evaluate the robustness of the results. Reverse MR analysis was also applied to investigate potential reverse causality.

Through MR analysis, we identified 17 gut microbiota classifications that are closely associated with chronic sinusitis. However, after Bonferroni multiple correction, only class Bacilli (odds ratio: 0.785, 95% confidence interval: 0.677-0.911, p = .001, false discovery rate = 0.023) maintained a significant causal negative relationship with chronic sinusitis. Sensitivity analysis did not reveal any evidence of heterogeneity or horizontal pleiotropy. Reverse MR analysis found five gut microbiota classifications that are significantly associated with chronic sinusitis, but they were no longer significant after Bonferroni multiple correction. There was no evidence to suggest a reverse causal relationship between chronic sinusitis and class Bacilli.

Specific gut microbiota predicted by genetics exhibit a potential causal relationship with chronic sinusitis, and class Bacilli may have a protective effect on chronic sinusitis.

Bamboo shoot has long been regarded as a nutritious and healthy food. It is low in calorie and rich in high-quality dietary fiber (DF), making them a potential DF resource. However, the protective mechanism of soluble dietary fibers from Dendrocalamus brandisii (Munro) Kurz shoot (DS-SDF) on methionine and choline deficient (MCD) diet-induced non-alcoholic fatty liver disease (NAFLD) is still unclear. This study was aimed to investigate the regulation of DS-SDF on gut microbiota in MCD diet-induced mice and its potential protective effect on liver injury. The NAFLD model was induced by the MCD diet for 8 weeks. Through observation of changes in liver function and gut microorganisms, it was found that DS-SDF supplementation could inhibit liver inflammation, improve liver injury, regulate the diversity of gut microorganisms, increase the abundance of beneficial bacteria and short-chain fatty acid-producing bacteria, and reverse the gut disorders induced by the MCD diet in mice. This study showed that DS-SDF supplementation could treat NAFLD by regulating gut microbiota composition, improving liver function, and inhibiting the inflammatory response. It might broaden the idea of high-value utilization of DS-SDF.

Inflammation is a complex process that usually refers to the general response of the body to the harmful stimuli of various pathogens, tissue damage, or exogenous pollutants. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor that regulates cellular defense against oxidative damage and toxicity by expressing genes related to oxidative stress response and drug detoxification. In addition to its antioxidant properties, Nrf2 is involved in many other important physiological processes, including inflammation and metabolism. Nrf2 can bind the promoters of antioxidant genes and upregulates their expressions, which alleviate oxidation-induced inflammation. Nrf2 has been shown to upregulate heme oxygenase-1 expression, which promotes NF-κB activation and is closely related with inflammation. Nrf2, as a key factor in antioxidant response, is closely related to the expressions of pro-inflammatory factors, NF-κB pathway and cell metabolism. Bioactive peptides come from a wide range of sources and have many biological functions. Increasing evidence indicates that bioactive peptides have potential anti-inflammatory activities. This article summarized the sources, absorption and utilization of bioactive peptides and their role in alleviating inflammation via Nrf2 pathway. Bioactive peptides can also regulate gut microbiota and alter metabolites, which regulates the Nrf2 pathway through novel pathway and supplement the anti-inflammatory mechanisms of bioactive peptides. This review provides a reference for further study on the anti-inflammatory effect of bioactive peptides and the development and utilization of functional foods.

The composition of mammalian gut microbiomes is highly conserved within species, yet the mechanisms by which microbiome composition is transmitted and maintained within lineages of wild animals remain unclear. Mutually compatible hypotheses exist, including that microbiome fidelity results from inherited dietary habits, shared environmental exposure, morphophysiological filtering and/or maternal effects. Interspecific hybrids are a promising system in which to interrogate the determinants of microbiome composition because hybrids can decouple traits and processes that are otherwise co-inherited in their parent species. We used a population of free-living hybrid zebras (Equus quagga × grevyi) in Kenya to evaluate the roles of these four mechanisms in regulating microbiome composition. We analysed faecal DNA for both the trnL-P6 and the 16S rRNA V4 region to characterize the diets and microbiomes of the hybrid zebra and of their parent species, plains zebra (E. quagga) and Grevy's zebra (E. grevyi). We found that both diet and microbiome composition clustered by species, and that hybrid diets and microbiomes were largely nested within those of the maternal species, plains zebra. Hybrid microbiomes were less variable than those of either parent species where they co-occurred. Diet and microbiome composition were strongly correlated, although the strength of this correlation varied between species. These patterns are most consistent with the maternal-effects hypothesis, somewhat consistent with the diet hypothesis, and largely inconsistent with the environmental-sourcing and morphophysiological-filtering hypotheses. Maternal transmittance likely operates in conjunction with inherited feeding habits to conserve microbiome composition within species.

To investigate the incidence and clinical impact of occult bacteremia in liver transplantation (LT).

This prospective observational study involved a fixed-point observation for up to 2 weeks after living donor LT in 20 recipients, with 20 donors as comparison subjects. Bacteria in the blood samples were detected using the ribosomal RNA-targeted reverse-transcription quantitative polymerase chain reaction method. To identify the causality with the gut microbiota (GM), fecal samples were collected and analyzed simultaneously.

Occult bacteremia was identified in four recipients (20%) and three donors (15%) before the operation, and in seven recipients (35%) and five donors (25%) after the operation. Clostridium leptum subgroup, Prevotella, Colinesella, Enterobacteriaceae, and Streptococcus were the main pathogens responsible. Although it did not negatively affect the donor post-hepatectomy outcomes, the recipients with occult bacteremia had a higher rate of infectious complications post-LT. The GM analyses showed fewer post-LT predominant obligate anaerobes in both the recipients and donors with occult bacteremia.

Occult bacteremia is a common condition that occurs in both donors and recipients. While occult bacteremia generally remains subclinical in the healthy population, there is potential risk of the development of an apparent post-LT infection in recipients who are highly immunosuppressed.

Chronic kidney disease (CKD) is a widespread health concern, which affects ~9.1% of the global population and 12-15% of individuals in upper-middle income countries. Notably, ~2% of patients with CKD progress to end-stage renal disease (ESRD), which leads to a substantial decline in the quality of life, an increased risk of mortality and significant financial burden. Patients with ESRD often still suffer from uremia and uremic syndromes, due to the accumulation of toxins between dialysis sessions and the inadequate removal of protein-bound toxins during dialysis. A number of these toxins are produced by the gut microbiota through the fermentation of dietary proteins or cholines. Furthermore, the gut microbial community serves a key role in maintaining metabolic and immune equilibrium in individuals. The present study aimed to investigate the gut microbiota patterns in individuals with type 2 diabetes mellitus (T2DM) and ESRD via quantitative PCR analysis of the 16S and 18S ribosomal RNA of selected members of the gut microbiota. Individuals affected by both T2DM and ESRD displayed distinctive features within their intestinal microbiota. Specifically, there were increased levels of Gammaproteobacteria observed in these patients, and all subjects exhibited a notably increased presence of Enterobacteriaceae compared with healthy individuals. This particular microbial community has established connections with the presence of inflammatory processes in the colon. Moreover, the elevated levels of Enterobacteriaceae may serve as an indicator of an imbalance in the intestinal microbiota, a condition known as dysbiosis. In addition, the Betaproteobacteria phylum was significantly more prevalent in the stool samples of patients with both T2DM and ESRD when compared with the control group. In conclusion, the present pilot study focused on gut microbiome alterations in T2DM and ESRD. Understanding the relationship between dysbiosis and CKD may identify new areas of research and therapeutic interventions aimed at modulating the gut microbiota to improve the health and outcomes of individuals with CKD and ESRD.

Live biotherapeutic product (LBP), a type of biological product, holds promise for the prevention or treatment of metabolic disease and pathogenic infection. Probiotics are live microorganisms that improve the intestinal microbial balance and beneficially affect the health of the host when ingested in sufficient numbers. These biological products possess the advantages of inhibition of pathogens, degradation of toxins, and modulation of immunity. The application of LBP and probiotic delivery systems has attracted great interest to researchers. The initial used technologies for LBP and probiotic encapsulation are traditional capsules and microcapsules. However, the stability and targeted delivery capability require further improved. The specific sensitive materials can greatly improve the delivery efficiency of LBPs and probiotics. The specific sensitive delivery systems show advantages over traditional ones due to their better properties of biocompatibility, biodegradability, innocuousness, and stability. Moreover, some new technologies, including layer-by-layer encapsulation, polyelectrolyte complexation, and electrohydrodynamic technology, show great potential in LBP and probiotic delivery. In this review, novel delivery systems and new technologies of LBPs and probiotics were presented, and the challenges and prospects were explored in specific sensitive materials for LBP and probiotic delivery.

Inflammatory bowel disease (IBD), a continuum of chronic inflammatory diseases, is tightly associated with immune system dysregulation and dysbiosis, leading to inflammation in the gastrointestinal tract (GIT) and multiple extraintestinal manifestations. The pathogenesis of IBD is not completely elucidated. However, it is associated with an increased risk of colorectal cancer (CRC), which is one of the most common gastrointestinal malignancies. In both IBD and CRC, a complex interplay occurs between the immune system and gut microbiota (GM), leading to the alteration in GM composition. Melatonin, a neuroendocrine hormone, was found to be involved with this interplay, especially since it is present in high amounts in the gut, leading to some protective effects. Actually, melatonin enhances the integrity of the intestinal mucosal barrier, regulates the immune response, alleviates inflammation, and attenuates oxidative stress. Thereby, the authors summarize the multifactorial interaction of melatonin with IBD and with CRC, focusing on new findings related to the mechanisms of action of this hormone, in addition to its documented positive outcomes on the treatment of these two pathologies and possible future perspectives to use melatonin as an adjuvant therapy.

It is hypothesized that COVID-19, post-COVID and post-mRNA COVID-19 (and other related) vaccine manifestations including "long haul syndrome" are due to deficiency of essential fatty acids (EFAs) and dysregulation of their metabolism. This proposal is based on the observation that EFAs and their metabolites can modulate the swift immunostimulatory response of SARS-CoV-2 and similar enveloped viruses, suppress inappropriate cytokine release, possess cytoprotective action, modulate serotonin and bradykinin production and other neurotransmitters, inhibit NF-kB activation, regulate cGAS-STING pathway, modulate gut microbiota, inhibit platelet activation, regulate macrophage and leukocyte function, enhance wound healing and facilitate tissue regeneration and restore homeostasis. This implies that administration of EFAs could be of benefit in the prevention and management of COVID-19 and its associated complications.

Osteoarthritis (OA) is a common degenerative joint disease that can cause severe pain, motor dysfunction, and even disability. A growing body of research indicates that gut microbiota and their associated metabolites are key players in maintaining bone health and in the progression of OA. Short-chain fatty acids (SCFAs) are a series of active metabolites that widely participate in bone homeostasis. Gold nanoparticles (GNPs) with outstanding anti-bacterial and anti-inflammatory properties, have been demonstrated to ameliorate excessive bone loss during the progression of osteoporosis (OP) and rheumatoid arthritis (RA). However, the protective effects of GNPs on OA progression are not clear. Here, we observed that GNPs significantly alleviated anterior cruciate ligament transection (ACLT)-induced OA in a gut microbiota-dependent manner. 16S rDNA gene sequencing showed that GNPs changed gut microbial diversity and structure, which manifested as an increase in the abundance of Akkermansia and Lactobacillus. Additionally, GNPs increased levels of SCFAs (such as butyric acid), which could have improved bone destruction by reducing the inflammatory response. Notably, GNPs modulated the dynamic balance of M1/M2 macrophages, and increased the serum levels of anti-inflammatory cytokines such as IL-10. To sum up, our study indicated that GNPs exhibited anti-osteoarthritis effects via modulating the interaction of "microbiota-gut-joint" axis, which might provide promising therapeutic strategies for OA.

The gut microbiota, often called the "forgotten organ," plays a crucial role in bidirectional communication with the host for optimal physiological function. This communication helps regulate the host's immunity and metabolism positively and negatively. Many factors influence microbiota homeostasis and subsequently lead to an immune system imbalance. The correlation between an unbalanced immune system and acute diseases such as acute kidney injury is not fully understood, and the role of gut microbiota in disease pathogenesis is still yet uncovered. This review summarizes our understanding of gut microbiota, focusing on the interactions between the host's immune system and the microbiome and their impact on acute kidney injury.

Polygonatum sibiricum is a plant with medicinal and nutritional properties. Saponins are the important biologically active components of Polygonatum sibiricum. In this study, the specific components of Polygonatum sibiricum saponins (PSS) were analyzed, and the regulation effect of PSS on intestinal flora in patients with ulcerative colitis (UC) was investigated by inducing male Kunming mice with dextran sulfate sodium (DSS). PSS could ameliorate the symptoms of weight loss, high DAI score and colon length reduction compared to DSS-induced treatment. Colonic fragments were taken for H&E staining and histopathological scoring. PSS could significantly improve the pathological abnormality of colitis mice. 16S rRNA analysis showed that the intestinal microbial community of mice treated with DSS was significantly damaged. PSS could restore the richness and diversity of intestinal microbial flora, reduce the number of pathogenic bacteria, and increase the abundance of Lactobacillus spp. and Muribaculaceae, and improve the intestinal microbial flora disorder. Generally, PSS had an obvious effect in relieving colitis in mice. This study confirmed that Polygonatum sibiricum saponins play a therapeutic and palliative role in ulcerative colitis by regulating the microbiome balance.

Crohn's disease, a chronic inflammatory process of the gastrointestinal tract defined by flares and periods of remission, is increasing in incidence. Despite advances in multimodal medical therapy, disease progression often necessitates multiple operations with high morbidity. The inability to treat Crohn's disease successfully is likely in part because the etiopathogenesis is not completely understood; however, recent research suggests the gut microbiome plays a critical role. How traditional perioperative management, including bowel preparation and preoperative antibiotics, further changes the microbiome and affects outcomes is not well described, especially in Crohn's patients, who are unique given their immunosuppression and baseline dysbiosis. This paper aims to outline current knowledge regarding perioperative management of Crohn's disease, the evolving role of gut dysbiosis, and how the microbiome can guide perioperative considerations with special attention to perioperative antibiotics as well as treatment of Mycobacterium avium subspecies paratuberculosis. In conclusion, dysbiosis is common in Crohn's patients and may be exacerbated by malnutrition, steroids, narcotic use, diarrhea, and perioperative antibiotics. Dysbiosis is also a major risk factor for anastomotic leak, and special consideration should be given to limiting factors that further perturb the gut microbiota in the perioperative period.

The connection between cardiovascular illnesses and the gut microbiota has drawn more and more attention in recent years. According to research, there are intricate relationships between dietary elements, gut bacteria, and their metabolites that affect cardiovascular health. In this study, the role of gut microbiota in cardiovascular disorders is examined, with an emphasis on the cardiac consequences brought on by changes in gut microbiota. This essay discusses the gut-heart axis in depth and in detail. It talks about clinical research looking at how soy consumption, probiotic supplements, and dietary changes affected gut microbiota and cardiovascular risk variables. Our goal is to clarify the possible pathways that connect gut microbiota to cardiovascular health and the implications for upcoming treatment approaches. The authors examine the composition, roles, and effects of the gut microbiota on cardiovascular health, including their contributions to hypertension, atherosclerosis, lipid metabolism, and heart failure. Endotoxemia, inflammation, immunological dysfunction, and host lipid metabolism are some of the potential processes investigated for how the gut microbiota affects cardiac outcomes. The research emphasizes the need for larger interventional studies and personalized medicine strategies to completely understand the complexity of the gut-heart axis and its implications for the management of cardiovascular disease. The development of novel treatment strategies and cutting-edge diagnostic technologies in cardiovascular medicine may be facilitated by a better understanding of this axis.

Alcoholic-associated liver diseases (ALD) are now widespread issues worldwide. Alcoholic-induced chronic dysbiosis of the gut microbiota is one of the factors in the pathophysiology of ALD.

In this work, we employed a chronic-binge ethanol feeding mice model, as described in a previous report.

Our findings demonstrate that hepatic inflammatory injury damage and accumulation of fat can be effectively reduced in mice with ALD by altering the gut microbiota utilizing Bacillus coagulans. Treatment with B. coagulans significantly modulates the levels of TNF-α, IL-1β, and IL-22 cytokines while maintaining tight junction proteins and mucin protein expressions to support intestinal barrier function restoration. Treatment with B. coagulans also alters the composition of the gut microbiota and increases the production of short-chain fatty acids (SCFAs).

This is mostly due to B. coagulans promotes the growth of bacteria that produce SCFAs, such as Ruminococcus species and Akkermansia, while inhibiting the growth of pathogenic bacteria like Escherichia Shigella. Moreover, treatment with B. coagulans causes levels of 2-Ketobutyric acid, ketoleucine, and indoleacetic acid increase while homovanillic acid and 3'-O-Methylguanosine metabolites decrease significantly. This study facilitates the development of therapeutic and preventive strategies for ALD using lactic acid bacteria.