• butyrate
• dietary fiber
• immune homeostasis
• intestinal barrier function
• resistant starch
• secondary bile acids
• short-chain fatty acids

• Humans
• Gastrointestinal Microbiome/physiology
• Obesity/microbiology
• Dietary Fiber/administration & dosage
• Diet
• Fatty Acids, Volatile/metabolism
• Bile Acids and Salts/metabolism
• Diet, High-Fat/adverse effects

• Gut barrier
• Gut microbiome
• Inflammatory bowel disease
• Intestinal permeability

• Humans
• Gastrointestinal Microbiome
• Intestinal Mucosa/metabolism
• Intestinal Mucosa/physiopathology
• Permeability

• Colombia
• Spearman
• climate
• climatic variables
• correlation analysis
• correlation coefficient
• leishmania
• leishmaniasis

• Leishmaniasis, Cutaneous/epidemiology
• Leishmaniasis, Cutaneous/transmission
• Colombia/epidemiology
• Incidence
• Humans
• Climate Change
• Cities/epidemiology
• Animals
• Temperature
• Rain
• Climate

• Convocatoria Interna No. 01-2024. Universidad Santiago de Cali

• fermented feed
• gut
• metabolome
• microbiome
• squabs

• SPERT B21 SAAS Program for Excellent Research Team
• 202212 Wellcome Trust

• antibacterial peptide
• intestinal microorganisms
• piglets
• tannic acid
• zinc oxide

• Chronic inflammatory disease
• Microbiota
• Multiple sclerosis
• Probiotics

• controlled human infection model
• diarrhea
• enterotoxigenic Escherichia coli
• experimental infection in humans
• feces
• heat-stable enterotoxin
• quantitative PCR
• small intestine
• vaccine

• Anti-inflammatory
• broccoli
• colitis
• gut microbiota
• sulforaphane

• intestinal disease
• intestinal stem cell
• microbiota
• niche
• postbiotic

• National Natural Science Foundation of China

• colonocytes
• conventional diet
• gut microbiota
• immune response
• inositol phosphates
• phytate hydrolysate
• vegan diet

• Humans
• Phytic Acid/pharmacology
• Interleukin-10
• Interleukin-8
• Myeloid Differentiation Factor 88
• Toll-Like Receptor 4
• Bacteria
• Cytokines
• Immunity
• Mucins
• Neoplasms

• Acrylamide
• Barrier function
• Cytotoxicity
• Flavonol
• Heat treatment
• IEC-6 cells

• Acrylamide/toxicity
• Animals
• Flavonoids
• Hot Temperature
• Intestinal Mucosa/metabolism
• Quercetin/metabolism
• Quercetin/pharmacology
• Rats
• Tight Junctions/metabolism

Considered an artifact just after discovery, the possibility of oral delivery of extracellular vesicles (EVs) and their functional cargos has recently gained much research attention. EVs from various sources, including edible plants, milk, bacteria and mammalian cells, have emerged as a platform for miRNA and drug delivery that seem to induce the expected immune effects locally and in distant tissues after oral administration. Such a possibility greatly expands the clinical applicability of EVs. The present review summarizes research findings that either support or deny the biological/therapeutical activity of orally administered EVs and their role in cross-species and cross-kingdom signaling.

In recent years, modulation of gut microbiota through prebiotics has garnered interest as a potential to ameliorate intestinal barrier dysfunction. The aim of the study was to examine the in vitro effect of fermentation supernatants (FSs) from rich in β-glucan Pleurotus eryngii mushrooms on the expression levels of tight junctions (TJs) genes in Caco-2 cells stimulated by bacterial lipopolysaccharides (LPS). Mushrooms were fermented using fecal inocula in an in vitro batch culture model. Caco-2 cells were subjected to LPS and FS treatment under three different conditions: pre-incubation with FS, co- and post-incubation. Reverse transcription PCR was applied to measure the expression levels of zonulin-1, occludin and claudin-1 genes. FSs from P. eryngii mushrooms led to a significant upregulation of the TJs gene expression in pre-incubation state, indicating potential preventive action. Down-regulation of all TJs gene expression levels was observed when the cells were challenged with LPS. The FS negative control (gut microbiota of each donor with no carbohydrate source) exhibited a significant upregulation of TJs expression levels compared to the cells that were challenged with LPS, for all three conditions. Overall, our data highlighted the positive and potential protective effects of P. eryngii mushrooms in upregulation of TJs’ genes.

• Pleurotus eryngii
• claudin-1
• fermentation supernatants
• gut barrier
• occludin
• zonulin 1

Acute diarrhea in dogs is one of the most common reasons for veterinary visits. Although this disorder is generally self-limiting, antibiotics are still frequently used as treatment for acute diarrhea in clinical practice. Antimicrobial resistance represents a major challenge for public health and requires immediate and drastic solutions. To date, the emergence and spread of antimicrobial resistance has been attributed to the misuse or indiscriminate use of antibiotics. The aim of this study is to compare the effects on clinical activity and fecal microbiota of the administration of an antibiotic combination in comparison to a nutraceutical product in dogs with acute non-hemorrhagic diarrhea. The results of the present study suggest that this nutraceutical treatment had a similar clinical effect compared to the antibiotic formulation and may represent an alternative to commonly used antimicrobial therapy.

Dogs with acute diarrhea are often presented to clinical practice and, although this generally represents a self-limiting condition, antibiotics are still frequently used as treatment. The aim of this study was to evaluate the effects in dogs with acute non-hemorrhagic diarrhea of the administration of an antibiotic combination in comparison to a nutraceutical product. Thirty dogs were enrolled and randomly assigned to two groups: 15 dogs (group A) received a nutraceutical commercial product while 15 dogs (group B) received an antimicrobial combination of metronidazole and spiramycin. For each dog, the Canine Acute Diarrhea Severity Index, the fecal microbiota and the Dysbiosis Index were assessed. Both stool consistency and frequency decreased on day 2 in the dogs of group A compared to baseline, while in group B, these parameters significantly decreased at days 3 and 4. The global concern for rising antibiotic resistance associated with indiscriminate use of antimicrobials, in both humans and animals, suggests the necessity of avoiding empirical and injudicious use of these molecules in diarrheic dogs. These results suggest that the nutraceutical treatment had a similar clinical effect compared to the antibiotic formulation, representing a valid antibiotic-sparing therapeutic approach in canine acute diarrhea.

• Canine Acute Diarrhea Severity Index
• Dysbiosis Index
• acute diarrhea
• antibiotic-sparing therapy
• antimicrobial resistance
• dog
• gut microbiota
• nutraceutical

Epithelial damage and loss of barrier integrity occur following intestinal infections in humans and animals. Gut health was evaluated by electron microscopy in an avian model that exposed birds to subclinical necrotic enteritis (NE) and fed them a diet supplemented with the probiotic Bacillus amyloliquefaciens strain H57 (H57). Scanning electron microscopy of ileal mucosa revealed significant villus damage, including focal erosions of epithelial cells and villous atrophy, while transmission electron microscopy demonstrated severe enterocyte damage and loss of cellular integrity in NE-exposed birds. In particular, mitochondria were morphologically altered, appearing irregular in shape or swollen, and containing electron-lucent regions of matrix and damaged cristae. Apical junctional complexes between adjacent enterocytes were significantly shorter, and the adherens junction was saccular, suggesting loss of epithelial integrity in NE birds. Segmented filamentous bacteria attached to villi, which play an important role in intestinal immunity, were more numerous in birds exposed to NE. The results suggest that mitochondrial damage may be an important initiator of NE pathogenesis, while H57 maintains epithelium and improves the integrity of intestinal mucosa. Potential actions of H57 are discussed that further define the mechanisms responsible for probiotic bacteria’s role in maintaining gut health.

Fructooligosaccharides (FOS) can change gut microbiota composition and play a protective role in food allergy (FA).

• Eucheuma serra
• Food allergy
• Intestinal microbiota
• Ovalbumin
• Sulfated polysaccharide

Growing experimental and clinical evidence suggests that a chronic inflammatory response induced by gut dysbiosis can critically contribute to the development of rheumatic diseases, including rheumatoid arthritis (RA). Of interest, an adherence to a Mediterranean diet has been linked to a reduction in mortality and morbidity in patients with inflammatory diseases. Diet and intestinal microbiota are modifying factors that may influence intestinal barrier strength, functional integrity, and permeability regulation. Intestinal microbiota may play a crucial role in RA pathogenesis, but up to now no solid data has clarified a mechanistic relationship between gut microbiota and the development of RA. Nonetheless, microbiota composition in subjects with RA differs from that of controls and this altered microbiome can be partially restored after prescribing disease modifying antirheumatic drugs. High levels of Prevotella copri and similar species are correlated with low levels of microbiota previously associated with immune regulating properties. In addition, some nutrients can alter intestinal permeability and thereby influence the immune response without a known impact on the microbiota. However, critical questions remain to be elucidated, such as the way microbiome fluctuates in relation to diet, and how disease activity may be influenced by changes in diet, microbiota or diet-intestinal microbiota equilibrium.

• Mediterranean Diet
• diet
• gut microbiota
• gut permeability
• rheumatoid arthritis

To evaluate the efficacy and safety of Tongfu powder for external application on Shénquè (the umbilicus, hereafter, Tongfu powder) versus mosapride in acute pancreatitis (AP) patients with gastrointestinal dysfunction.

A total of 102 AP patients were diagnosed using the latest Atlanta Criterion and recruited at the Department of Infectious Disease, Beijing Friendship Hospital (Beijing, People’s Republic of China) from August 2014 to December 2016. Patients were randomized into the Tongfu powder group and mosapride group using the random table. Information on scores (eg, the gastrointestinal function score) on days 1 and 7 of hospitalization, biochemical indicators (eg, interleukin [IL]-2 and IL-6), indicators for curative effects (eg, first defecation time, bowel sound recovery time, hospitalization costs, and duration) were collected and compared between the 2 groups.

The gastrointestinal function score decreased significantly after treatment, and the changes were significantly different between the Tongfu powder group and the mosapride group (P<0.05). Significantly shorter time to first defecation and bowel sound recovery was observed in the Tongfu powder group versus the mosapride group (P<0.05). The improvements of IL-2, IL-4, intestinal fatty acid binding protein, motilin, and vasoactive intestinal peptide in the Tongfu powder group were higher than those in the mosapride group (P<0.05). There were no significant differences in hospital cost and length of hospital stay between the 2 groups.

This study suggested that Tongfu powder for external application may improve gastrointestinal function for AP patients compared with mosapride.

• Tongfu powder
• acute pancreatitis
• gastrointestinal dysfunction
• mosapride

• Autoimmune Diseases/epidemiology
• Autoimmune Diseases/metabolism
• Autoimmune Diseases/microbiology
• Blood Group Antigens/metabolism
• Cardiovascular Diseases/epidemiology
• Cardiovascular Diseases/metabolism
• Cardiovascular Diseases/microbiology
• Diabetes Mellitus/epidemiology
• Diabetes Mellitus/metabolism
• Diabetes Mellitus/microbiology
• Gastrointestinal Microbiome
• Humans
• Inflammation/epidemiology
• Inflammation/metabolism
• Inflammation/microbiology
• Obesity/epidemiology
• Obesity/metabolism
• Obesity/microbiology

• U24 DK097193 NIDDK NIH HHS

• Immune response
• Immunity
• Immunology and Microbiology Section
• antibiotic alternative
• bacterial composition and distribution
• grape seed proanthocyanidins
• intestinal mucosal barrier
• oxidative stress

• Dietary modulation
• Epithelium physiology
• G-protein-coupled receptors
• Histone deacetylases
• Microbe–host interactions
• Rumen microbiota

• Animal Feed/analysis
• Animals
• Dietary Carbohydrates/metabolism
• Dietary Fiber/metabolism
• Epithelium/microbiology
• Epithelium/physiology
• Fermentation
• Gastrointestinal Microbiome/genetics
• Gastrointestinal Microbiome/physiology
• Goats/metabolism
• Goats/microbiology
• High-Throughput Nucleotide Sequencing
• Histone Deacetylases/genetics
• Histone Deacetylases/metabolism
• RNA, Ribosomal, 16S/metabolism
• Receptors, G-Protein-Coupled/genetics
• Receptors, G-Protein-Coupled/metabolism
• Rumen/cytology
• Rumen/microbiology
• Rumen/physiology
• Transcriptome

• the Chinese National“973” Project
• Project Grant Natural Science Foundation of Jiangsu Province
• Independent Innovation Project of Nanjing Agriculture University
• Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)

• Gut microbiota
• Immune system
• Intestinal permeability
• Nanoparticle
• Polymer
• Surfactant

Malnutrition and rotavirus infection, prevalent in developing countries, individually and in combination, affect the health of millions of children, compromising their immunity and increasing the rates of death from infectious diseases. However, the interactions between the two and their combined effects on immune and intestinal functions are poorly understood. We have established the first human infant microbiota-transplanted neonatal pig model of childhood malnutrition that reproduced the impaired immune, intestinal, and other physiological functions seen in malnourished children. This model can be used to evaluate relevant dietary and other health-promoting interventions. Our findings provide an explanation of why adequate nutrition alone may lack efficacy in malnourished children.

Malnutrition affects millions of children in developing countries, compromising immunity and contributing to increased rates of death from infectious diseases. Rotavirus is a major etiological agent of childhood diarrhea in developing countries, where malnutrition is prevalent. However, the interactions between the two and their combined effects on immune and intestinal functions are poorly understood. In this study, we used neonatal gnotobiotic (Gn) pigs transplanted with the fecal microbiota of a healthy 2-month-old infant (HIFM) and fed protein-deficient or -sufficient bovine milk diets. Protein deficiency induced hypoproteinemia, hypoalbuminemia, hypoglycemia, stunting, and generalized edema in Gn pigs, as observed in protein-malnourished children. Irrespective of the diet, human rotavirus (HRV) infection early, at HIFM posttransplantation day 3 (PTD3), resulted in adverse health effects and higher mortality rates (45 to 75%) than later HRV infection (PTD10). Protein malnutrition exacerbated HRV infection and affected the morphology and function of the small intestinal epithelial barrier. In pigs infected with HRV at PTD10, there was a uniform decrease in the function and/or frequencies of natural killer cells, plasmacytoid dendritic cells, and CD103⁺ and apoptotic mononuclear cells and altered gene expression profiles of intestinal epithelial cells (chromogranin A, mucin 2, proliferating cell nuclear antigen, SRY-Box 9, and villin). Thus, we have established the first HIFM-transplanted neonatal pig model that recapitulates major aspects of protein malnutrition in children and can be used to evaluate physiologically relevant interventions. Our findings provide an explanation of why nutrient-rich diets alone may lack efficacy in malnourished children.

IMPORTANCE Malnutrition and rotavirus infection, prevalent in developing countries, individually and in combination, affect the health of millions of children, compromising their immunity and increasing the rates of death from infectious diseases. However, the interactions between the two and their combined effects on immune and intestinal functions are poorly understood. We have established the first human infant microbiota-transplanted neonatal pig model of childhood malnutrition that reproduced the impaired immune, intestinal, and other physiological functions seen in malnourished children. This model can be used to evaluate relevant dietary and other health-promoting interventions. Our findings provide an explanation of why adequate nutrition alone may lack efficacy in malnourished children.

• gnotobiotic piglets
• human infant fecal microbiota
• human rotavirus
• innate immunity
• intestinal epithelial barrier
• intestinal epithelial cells
• natural killer cells
• plasmacytoid dendritic cells
• protein deficiency

• Beta-Hydroxybutyrate
• GPR109a
• HCA(2)
• Inflammation
• Niacin

• Animals
• Atherosclerosis/prevention & control
• Colitis/prevention & control
• Diabetic Retinopathy/prevention & control
• Humans
• Inflammation/prevention & control
• Mice
• Neoplasms/prevention & control
• Neurodegenerative Diseases/prevention & control
• Niacin/therapeutic use
• Obesity/prevention & control
• Receptors, G-Protein-Coupled/analysis
• Receptors, G-Protein-Coupled/physiology
• Receptors, Nicotinic/analysis
• Receptors, Nicotinic/physiology

The intestinal tract represents the largest interface between the external environment and the human body. Nutrient uptake mostly happens in the intestinal tract, where the epithelial surface is constantly exposed to dietary antigens. Since inflammatory response toward these antigens may be deleterious for the host, a plethora of protective mechanisms take place to avoid or attenuate local damage. For instance, the intestinal barrier is able to elicit a dynamic response that either promotes or impairs luminal antigens adhesion and crossing. Regulation of intestinal barrier is crucial to control intestinal permeability whose increase is associated with chronic inflammatory conditions. The cross talk among bacteria, immune, and dietary factors is able to modulate the mucosal barrier function, as well as the intestinal permeability. Several nutritional products have recently been proposed as regulators of the epithelial barrier, even if their effects are in part contradictory. At the same time, the metabolic function of the microbiota generates new products with different effects based on the dietary content. Besides conventional treatments, novel therapies based on complementary nutrients are now growing. Fecal therapy has been recently used for the clinical treatment of refractory Clostridium difficile infection instead of the classical antibiotic therapy. In the present review, we will outline the epithelial response to nutritional components derived from dietary intake and microbial fermentation focusing on the consequent effects on the integrity of the epithelial barrier.

• inflammation
• intestinal permeability
• microbiota
• mucosal immunity
• nutrition

• dysautonomia
• epigenetics
• food allergy
• gluten-related disorders
• gut-brain axis
• microbiome

The incidence of obesity and its related conditions, including non-alcoholic fatty liver disease (NAFLD), has dramatically increased in all age groups worldwide. Given the health consequences of these conditions, and the subsequent economic burden on healthcare systems, their prevention and treatment have become major priorities. Because standard dietary and lifestyle changes and pathogenically-oriented therapies (e.g., antioxidants, oral hypoglycemic agents, and lipid-lowering agents) often fail due to poor compliance and/or lack of efficacy, novel approaches directed toward other pathomechanisms are needed. Here we present several lines of evidence indicating that, by increasing energy extraction in some dysbiosis conditions or small intestinal bacterial overgrowth, specific gut microbiota and/or a “low bacterial richness” may play a role in obesity, metabolic syndrome, and fatty liver. Under conditions involving a damaged intestinal barrier (“leaky gut”), the gut-liver axis may enhance the natural interactions between intestinal bacteria/bacterial products and hepatic receptors (e.g., toll-like receptors), thus promoting the following cascade of events: oxidative stress, insulin-resistance, hepatic inflammation, and fibrosis. We also discuss the possible modulation of gut microbiota by probiotics, as attempted in NAFLD animal model studies and in several pilot pediatric and adult human studies. Globally, this approach appears to be a promising and innovative add-on therapeutic tool for NAFLD in the context of multi-target therapy.

• Probiotics
• Gut-liver axis
• Intestinal microbiota
• Barrier function
• Small intestinal bacterial overgrowth
• Bacterial translocation
• Non-alcoholic fatty liver disease

• Animals
• Bacterial Translocation
• Disease Models, Animal
• Dysbiosis
• Host-Pathogen Interactions
• Humans
• Intestinal Mucosa/metabolism
• Intestines/microbiology
• Liver/metabolism
• Liver/microbiology
• Microbiota
• Non-alcoholic Fatty Liver Disease/diagnosis
• Non-alcoholic Fatty Liver Disease/metabolism
• Non-alcoholic Fatty Liver Disease/microbiology
• Non-alcoholic Fatty Liver Disease/therapy
• Probiotics/therapeutic use
• Signal Transduction
• Treatment Outcome

Toll-like receptors (TLRs) recognize microbial pathogens and trigger immune response, but their regulation by neuropeptide-vasoactive intestinal peptide (VIP) in weaned piglets infected by enterotoxigenic Escherichia coli (ETEC) K88 remains unexplored. Therefore, the study was conducted to investigate its role using a model of early weaned piglets infected by ETEC K88. Male Duroc×Landrace×Yorkshire piglets (n = 24) were randomly divided into control, ETEC K88, VIP, and ETEC K88+VIP groups. On the first three days, ETEC K88 and ETEC K88+VIP groups were orally administrated with ETEC K88, other two groups were given sterile medium. Then each piglet from VIP and ETEC K88+VIP group received 10 nmol VIP intraperitoneally (i.p.) once daily, on day four and six. On the seventh day, the piglets were sacrificed. The results indicated that administration of VIP improved the growth performance, reduced diarrhea incidence of ETEC K88 challenged pigs, and mitigated the histopathological changes of intestine. Serum levels of IL-2, IL-6, IL-12p40, IFN-γ and TNF-α in the ETEC K88+ VIP group were significantly reduced compared with those in the ETEC group. VIP significantly increased IL-4, IL-10, TGF-β and S-IgA production compared with the ETEC K88 group. Besides, VIP could inhibit the expression of TLR2, TLR4, MyD88, NF-κB p65 and the phosphorylation of IκB-α, p-ERK, p-JNK, and p-38 induced by ETEC K88. Moreover, VIP could upregulate the expression of occludin in the ileum mucosa compared with the ETEC K88 group. Colon and caecum content bacterial richness and diversity were lower for pigs in the ETEC group than the unchallenged groups. These results demonstrate that VIP is beneficial for the maturation of the intestinal mucosal immune system and elicited local immunomodulatory activities. The TLR2/4-MyD88 mediated NF-κB and MAPK signaling pathway may be critical to the mechanism underlying the modulatory effect of VIP on intestinal mucosal immune function and bacterial community.

• Antioxidant genes
• Date palm fruit extracts
• Gilthead seabream (Sparus aurata L.)
• Probiotics
• Teleosts

• Animals
• Catalase/metabolism
• DNA Primers/genetics
• Dietary Supplements
• Gene Expression Regulation, Enzymologic/drug effects
• Glutathione Reductase/metabolism
• Mucous Membrane/drug effects
• Mucous Membrane/metabolism
• Phoeniceae/chemistry
• Plant Extracts/pharmacology
• Probiotics/pharmacology
• Real-Time Polymerase Chain Reaction
• Sea Bream/metabolism
• Superoxide Dismutase/metabolism

The human microbiome consist of the composite genome of native flora that have evolved with humanity over millennia and which contains 150-fold more genes than the human genome. A “healthy” microbiome plays an important role in the maintenance of health and prevention of illness, inclusive of autoimmune disease such as inflammatory bowel disease (IBD). IBD is a prevalent spectrum of disorders, most notably defined by Crohn’s disease (CD) and ulcerative colitis (UC), which are associated with considerable suffering, morbidity, and cost. This review presents an outline of the loss of a normal microbiome as an etiology of immune dysregulation and IBD pathogenesis initiation. We, furthermore, summarize the knowledge on the role of a healthy microbiome in terms of its diversity and important functional elements and, lastly, conclude with some of the therapeutic interventions and modalities that are now being explored as potential applications of microbiome-host interactions.

• cell differentiation
• cystic fibrosis
• epithelial injury
• host-pathogen interactions
• microbiome
• three-dimensional