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Dong Y, Zhang L, Qiu D, Yao R, Jia H, Wang H, Zhou L, Zhang J, Zhang N. Lactobacillus murinus ZNL-13 Modulates Intestinal Barrier Damage and Gut Microbiota in Cyclophosphamide-Induced Immunosuppressed Mice. Foods 2025; 14:1416. [PMID: 40282817 PMCID: PMC12026897 DOI: 10.3390/foods14081416] [Citation(s) in RCA: 1] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/24/2025] [Revised: 04/14/2025] [Accepted: 04/17/2025] [Indexed: 04/29/2025] Open
Abstract
Cyclophosphamide (CTX) is a widely used anticancer drug in clinical practice; however, its administration can lead to gastrointestinal damage and immune suppression. Lactobacillus murinus (L. murinus) has been shown to regulate immune cell activity and protect the gastrointestinal system, showing potential application as a functional food. The objective of this study was to investigate the effects of L. murinus ZNL-13 on CTX-induced intestinal mucosal injury and gut microbiota in mice. The results demonstrated that L. murinus ZNL-13 significantly alleviated weight loss and intestinal pathological damage. Moreover, in CTX-induced intestinal injury mice, L. murinus ZNL-13 enhanced the release of immune factors, suppressed cell apoptosis, and protected the intestinal mucosal barrier. Additionally, it activated the TLR4/NF-κB pathway, thereby promoting immune cell activity. Furthermore, L. murinus ZNL-13 contributed to the restoration of gut microbial homeostasis by increasing the relative abundance of short-chain fatty acid-producing bacteria. Taken together, this investigation highlights the potential of L. murinus ZNL-13 in protecting the intestinal barrier and enhancing immune function while laying the groundwork for its development as a novel probiotic and functional food.
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Affiliation(s)
- Yihan Dong
- College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; (Y.D.); (L.Z.); (D.Q.); (R.Y.); (H.J.); (H.W.); (L.Z.)
- Heilongjiang Provincial Key Laboratory of Pathogenic Mechanism for Animal Disease and Comparative Medicine, Harbin 150030, China
| | - Luyao Zhang
- College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; (Y.D.); (L.Z.); (D.Q.); (R.Y.); (H.J.); (H.W.); (L.Z.)
| | - Di Qiu
- College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; (Y.D.); (L.Z.); (D.Q.); (R.Y.); (H.J.); (H.W.); (L.Z.)
| | - Renxin Yao
- College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; (Y.D.); (L.Z.); (D.Q.); (R.Y.); (H.J.); (H.W.); (L.Z.)
| | - Haitao Jia
- College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; (Y.D.); (L.Z.); (D.Q.); (R.Y.); (H.J.); (H.W.); (L.Z.)
| | - Haiyang Wang
- College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; (Y.D.); (L.Z.); (D.Q.); (R.Y.); (H.J.); (H.W.); (L.Z.)
| | - Luyao Zhou
- College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; (Y.D.); (L.Z.); (D.Q.); (R.Y.); (H.J.); (H.W.); (L.Z.)
| | - Jiantao Zhang
- College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; (Y.D.); (L.Z.); (D.Q.); (R.Y.); (H.J.); (H.W.); (L.Z.)
- Heilongjiang Provincial Key Laboratory of Pathogenic Mechanism for Animal Disease and Comparative Medicine, Harbin 150030, China
| | - Na Zhang
- College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; (Y.D.); (L.Z.); (D.Q.); (R.Y.); (H.J.); (H.W.); (L.Z.)
- Key Laboratory of Dairy Science, Ministry of Education, Northeast Agricultural University, Harbin 150030, China
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Karačić A, Zonjić J, Stefanov E, Radolović K, Starčević A, Renko I, Krznarić Ž, Ivančić M, Šatalić Z, Liberati Pršo AM. Short-Term Supplementation of Sauerkraut Induces Favorable Changes in the Gut Microbiota of Active Athletes: A Proof-of-Concept Study. Nutrients 2024; 16:4421. [PMID: 39771042 PMCID: PMC11677004 DOI: 10.3390/nu16244421] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/16/2024] [Revised: 12/13/2024] [Accepted: 12/15/2024] [Indexed: 01/11/2025] Open
Abstract
BACKGROUND Since the gut microbiota is important for athlete health and performance, its optimization is increasingly gaining attention in sports nutrition, for example, with whole fermented foods. Sauerkraut is a traditional fermented food rich in pro-, pre-, and postbiotics, which has not yet been investigated in the field of sports nutrition. METHODS To determine whether sauerkraut could be used for gut microbiota optimization in sports nutrition, a proof-of-concept study was conducted. The microbiota composition of organic pasteurized sauerkraut was analyzed, and then healthy active athletes were provided with the same sauerkraut for 10 days as an intervention. The effects of sauerkraut on the athlete's gut microbiota, laboratory parameters, and bowel function were assessed. RESULTS Significant changes in the gut microbiota composition were seen on taxonomic and functional levels, independent of baseline microbiota composition, even after short-term supplementation. Most notably, there was an increase in several health-promoting genera of the family Lachnospiraceae, as well as significant alterations in metabolic pathways regarding cell wall synthesis and the metabolism of nucleotide bases. An increase in the proportion of lymphocytes and a decrease in B12 vitamin levels was observed, as well as a risk of indigestion in certain athletes, which significantly resolved after seven days of supplementation in all athletes. It is unclear whether the observed effects are attributable to the sauerkraut's own microbiome or its pre- and postbiotics since it is a whole food. CONCLUSIONS Our study has demonstrated that the concept of whole fermented foods, such as sauerkraut, could potentially be feasible and effective in sports nutrition for gut microbiota optimization.
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Affiliation(s)
- Andrija Karačić
- Faculty of Food Technology and Biotechnology, University of Zagreb, Pierottijeva 6, 10000 Zagreb, Croatia; (A.K.); (J.Z.); (E.S.); (A.S.); (I.R.); (Z.Š.)
- The Gut Microbiome Center (CCM), Jablanska 82, 10000 Zagreb, Croatia
- Department of Internal Medicine, University Hospital “Sveti Duh”, Sveti Duh 64, 10000 Zagreb, Croatia;
| | - Jadran Zonjić
- Faculty of Food Technology and Biotechnology, University of Zagreb, Pierottijeva 6, 10000 Zagreb, Croatia; (A.K.); (J.Z.); (E.S.); (A.S.); (I.R.); (Z.Š.)
| | - Ena Stefanov
- Faculty of Food Technology and Biotechnology, University of Zagreb, Pierottijeva 6, 10000 Zagreb, Croatia; (A.K.); (J.Z.); (E.S.); (A.S.); (I.R.); (Z.Š.)
| | - Katja Radolović
- Faculty of Food Technology and Biotechnology, University of Zagreb, Pierottijeva 6, 10000 Zagreb, Croatia; (A.K.); (J.Z.); (E.S.); (A.S.); (I.R.); (Z.Š.)
| | - Antonio Starčević
- Faculty of Food Technology and Biotechnology, University of Zagreb, Pierottijeva 6, 10000 Zagreb, Croatia; (A.K.); (J.Z.); (E.S.); (A.S.); (I.R.); (Z.Š.)
| | - Ira Renko
- Faculty of Food Technology and Biotechnology, University of Zagreb, Pierottijeva 6, 10000 Zagreb, Croatia; (A.K.); (J.Z.); (E.S.); (A.S.); (I.R.); (Z.Š.)
| | - Željko Krznarić
- Department of Internal Medicine, Faculty of Medicine, University of Zagreb, 10000 Zagreb, Croatia;
| | - Matija Ivančić
- Department of Internal Medicine, University Hospital “Sveti Duh”, Sveti Duh 64, 10000 Zagreb, Croatia;
| | - Zvonimir Šatalić
- Faculty of Food Technology and Biotechnology, University of Zagreb, Pierottijeva 6, 10000 Zagreb, Croatia; (A.K.); (J.Z.); (E.S.); (A.S.); (I.R.); (Z.Š.)
| | - Ana-Marija Liberati Pršo
- Faculty of Food Technology and Biotechnology, University of Zagreb, Pierottijeva 6, 10000 Zagreb, Croatia; (A.K.); (J.Z.); (E.S.); (A.S.); (I.R.); (Z.Š.)
- Department of Internal Medicine, University Hospital “Sveti Duh”, Sveti Duh 64, 10000 Zagreb, Croatia;
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Du W, Zhao Y, Zhang C, Zhang L, Zhou L, Sun Z, Huang X, Zhang N, Liu Z, Li K, Che N. Association of bacteriomes with drug susceptibility in lesions of pulmonary tuberculosis patients. Heliyon 2024; 10:e37583. [PMID: 39309911 PMCID: PMC11414563 DOI: 10.1016/j.heliyon.2024.e37583] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/24/2024] [Revised: 09/03/2024] [Accepted: 09/05/2024] [Indexed: 09/25/2024] Open
Abstract
Understanding how the bacteriomes in tuberculous lesions can be influenced by the susceptibility of Mycobacterium tuberculosis (MTB) can provide valuable information for preventing and treating drug resistant tuberculosis (DR-TB). High-throughput 16S rRNA sequencing was employed to analyze the bacteriome in pulmonary TB lesions from 14 patients with DR-TB and 47 patients with drug sensitive tuberculosis (DS-TB), along with 18 normal lung tissues (NT) from 18 lung cancer patients serving as the bacterial baseline. The phylogenetic investigation of communities by reconstruction of unobserved states2 (PICRUSt2) algorithm was utilized to predict bacterial metabolic functions. The major phyla of pulmonary bacteriomes included Proteobacteria, Actinobacteria, Bacteroidetes, Firmicutes and Fusobacteria. Alpha diversity indices, including ACE, Chao1, Shannon and OTU observed, all demonstrated different bacterial communities of DS-TB samples from that of NT samples; while only Shannon indicated difference between DR-TB and NT samples. The analysis of similarity (ANOSIM) showed significantly different bacterial communities within TB lesions compared to NT samples (R = 0.418, p = 0.001). However, difference was not observed between DR-TB and DS-TB samples (ANOSIM, R = 0.069, p = 0.173). The bacterial profiles within each DR-TB individual appeared unique, with no obvious clusters corresponding to drug-resistant phenotypes. Nevertheless, indicator genera identified in DR-TB and DS-TB lesions demonstrated distinctive micro-ecological environments. Most COG functions were enriched in TB lesions, and the most significant one was [J] translation, ribosomal structure and biogenesis. The distinct enrichment patterns of bacterial enzymes in DR-TB and DS-TB lesions suggest that pulmonary bacterial activities can be modulated by the susceptibility of MTB bacilli. This study provides fresh perspectives and strategies for the precise diagnosis and assessment of drug resistance tuberculosis.
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Affiliation(s)
- Weili Du
- Department of Pathology, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beiguandajie 9#, Tongzhou Dist, Beijing, 101149, China
| | - Yingli Zhao
- Department of Pathology, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beiguandajie 9#, Tongzhou Dist, Beijing, 101149, China
| | - Chen Zhang
- Department of Pathology, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beiguandajie 9#, Tongzhou Dist, Beijing, 101149, China
| | - Li Zhang
- Department of Pathology, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beiguandajie 9#, Tongzhou Dist, Beijing, 101149, China
| | - Lijuan Zhou
- Department of Pathology, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beiguandajie 9#, Tongzhou Dist, Beijing, 101149, China
| | - Zuyu Sun
- Department of Pathology, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beiguandajie 9#, Tongzhou Dist, Beijing, 101149, China
| | - Xiaojie Huang
- Department of Pathology, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beiguandajie 9#, Tongzhou Dist, Beijing, 101149, China
| | - Nana Zhang
- Department of Pathology, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beiguandajie 9#, Tongzhou Dist, Beijing, 101149, China
| | - Zichen Liu
- Department of Pathology, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beiguandajie 9#, Tongzhou Dist, Beijing, 101149, China
| | - Kun Li
- Department of Pathology, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beiguandajie 9#, Tongzhou Dist, Beijing, 101149, China
| | - Nanying Che
- Department of Pathology, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beiguandajie 9#, Tongzhou Dist, Beijing, 101149, China
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Vijayan S, Kandi V, Palacholla PS, Rajendran R, Jarugu C, Ca J, Pravallika M, Reddy SC, Sucharitha AS. Probiotics in Allergy and Immunological Diseases: A Comprehensive Review. Cureus 2024; 16:e55817. [PMID: 38590477 PMCID: PMC10999892 DOI: 10.7759/cureus.55817] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 03/08/2024] [Indexed: 04/10/2024] Open
Abstract
Allergy and immunological disorders like autoimmune diseases are vastly prevalent worldwide. These conditions account for a substantial amount of personal and social burden. Such illnesses have lengthy, uncertain, and spotted courses with unpredictable exacerbations. A definite tendency for improving the overall quality of life of individuals suffering from such diseases is crucial to tackling these diseases, especially through diet or lifestyle modification. Further, interventions like microbiome-based therapeutics such as prebiotics or probiotics were explored. Changes in the microbial population were evident during the flare-up of autoimmune and allergic conditions. The realization that the human microbiome is a central player in immunological diseases is a hallmark of its potential usefulness in therapy for such illnesses. This review focuses on the intricate symphony in the orchestra of the human microbiome and the immune system. New therapeutic strategies involving probiotics appear to be the future of personalized medicine. Through this review, we explore the narrative of probiotics and reaffirm their use as therapeutic and preventive agents in immunological disorders.
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Affiliation(s)
- Swapna Vijayan
- Pediatrics, Sir Chandrasekhara Venkata (CV) Raman General Hospital, Bangalore, IND
| | - Venkataramana Kandi
- Clinical Microbiology, Prathima Institute of Medical Sciences, Karimnagar, IND
| | - Pratyusha S Palacholla
- Internal Medicine, Vydehi Institute of Medical Sciences and Research Centre, Bangalore, IND
| | | | - Chandrasagar Jarugu
- General Practice, Vydehi Institute of Medical Sciences and Research Centre, Bangalore, IND
| | - Jayashankar Ca
- Internal Medicine, Vydehi Institute of Medical Sciences and Research Centre, Bangalore, IND
| | - Mundla Pravallika
- Internal Medicine, Vydehi Institute of Medical Sciences and Research Centre, Bangalore, IND
| | - Shruthi C Reddy
- Internal Medicine, Vydehi Institute of Medical Sciences and Research Centre, Bangalore, IND
| | - Atul S Sucharitha
- Internal Medicine, Vydehi Institute of Medical Sciences and Research Centre, Bangalore, IND
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Zhang X, Liu H, Hashimoto K, Yuan S, Zhang J. The gut–liver axis in sepsis: interaction mechanisms and therapeutic potential. Crit Care 2022; 26:213. [PMID: 35831877 PMCID: PMC9277879 DOI: 10.1186/s13054-022-04090-1] [Citation(s) in RCA: 69] [Impact Index Per Article: 23.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/25/2022] [Accepted: 07/09/2022] [Indexed: 12/20/2022] Open
Abstract
Sepsis is a potentially fatal condition caused by dysregulation of the body's immune response to an infection. Sepsis-induced liver injury is considered a strong independent prognosticator of death in the critical care unit, and there is anatomic and accumulating epidemiologic evidence that demonstrates intimate cross talk between the gut and the liver. Intestinal barrier disruption and gut microbiota dysbiosis during sepsis result in translocation of intestinal pathogen-associated molecular patterns and damage-associated molecular patterns into the liver and systemic circulation. The liver is essential for regulating immune defense during systemic infections via mechanisms such as bacterial clearance, lipopolysaccharide detoxification, cytokine and acute-phase protein release, and inflammation metabolic regulation. When an inappropriate immune response or overwhelming inflammation occurs in the liver, the impaired capacity for pathogen clearance and hepatic metabolic disturbance can result in further impairment of the intestinal barrier and increased disruption of the composition and diversity of the gut microbiota. Therefore, interaction between the gut and liver is a potential therapeutic target. This review outlines the intimate gut–liver cross talk (gut–liver axis) in sepsis.
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The Impacts of Iron Overload and Ferroptosis on Intestinal Mucosal Homeostasis and Inflammation. Int J Mol Sci 2022; 23:ijms232214195. [PMID: 36430673 PMCID: PMC9697168 DOI: 10.3390/ijms232214195] [Citation(s) in RCA: 21] [Impact Index Per Article: 7.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/21/2022] [Revised: 11/12/2022] [Accepted: 11/15/2022] [Indexed: 11/18/2022] Open
Abstract
Intestinal homeostasis is maintained through the interplay of the intestinal mucosa, local and systemic immune factors, and the microbial content of the gut. Iron is a trace mineral in most organisms, including humans, which is essential for growth, systemic metabolism and immune response. Paradoxically, excessive iron intake and/or high iron status can be detrimental to iron metabolism in the intestine and lead to iron overload and ferroptosis-programmed cell death mediated by iron-dependent lipid peroxidation within cell membranes, which contributes to several intestinal diseases. In this review, we comprehensively review recent findings on the impacts of iron overload and ferroptosis on intestinal mucosal homeostasis and inflammation and then present the progress of iron overload and ferroptosis-targeting therapy in intestinal diseases. Understanding the involved mechanisms can provide a new understanding of intestinal disease pathogenesis and facilitate advanced preventive and therapeutic strategies for intestinal dysfunction and diseases.
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Leceta J, Garin MI, Conde C. Mechanism of Immunoregulatory Properties of Vasoactive Intestinal Peptide in the K/BxN Mice Model of Autoimmune Arthritis. Front Immunol 2021; 12:701862. [PMID: 34335612 PMCID: PMC8322839 DOI: 10.3389/fimmu.2021.701862] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/28/2021] [Accepted: 06/25/2021] [Indexed: 11/13/2022] Open
Abstract
The K/BxN mouse model of rheumatoid arthritis (RA) closely resembles the human disease. In this model, arthritis results from activation of autoreactive KRN T cells recognizing the glycolytic enzyme glucose-6-phosphate isomerase (GPI) autoantigen, which provides help to GPI-specific B cells, resulting in the production of pathogenic anti-GPI antibodies that ultimately leads to arthritis symptoms from 4 weeks of age. Vasoactive intestinal peptide (VIP) is a neuropeptide broadly distributed in the central and peripheral nervous system that is also expressed in lymphocytes and other immune cell types. VIP is a modulator of innate and adaptive immunity, showing anti-inflammatory and immunoregulatory properties. Basically, this neuropeptide promotes a shift in the Th1/Th2 balance and enhances dedifferentiation of T regulatory cells (Treg). It has demonstrated its therapeutic effects on the collagen-induced arthritis (CIA) mouse model of RA. In the present hypothesis and theory article, we propose that the immunoregulatory properties of VIP may be due likely to the inhibition of T cell plasticity toward non-classic Th1 cells and an enhanced follicular regulatory T cells (Tfr) activity. The consequences of these regulatory properties are the reduction of systemic pathogenic antibody titers.
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Affiliation(s)
- Javier Leceta
- Department of Cell Biology, Faculty of Biology, Complutense University of Madrid, Madrid, Spain
| | - Marina I Garin
- Division of Hematopoietic Innovative Therapies, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas (CIEMAT) and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBER-ER), Madrid, Spain.,Advanced Therapy Unit, Instituto de Investigación Sanitaria Fundación Jiménez Díaz (IIS-FJD/UAM), Madrid, Spain
| | - Carmen Conde
- Laboratorio de Reumatología Experimental y Observacional, Instituto de Investigación Sanitaria de Santiago (IDIS), Hospital Clínico Universitario de Santiago de Compostela (CHUS), SERGAS, Santiago de Compostela, Spain
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The role of the microbiome in gastrointestinal inflammation. Biosci Rep 2021; 41:228872. [PMID: 34076695 PMCID: PMC8201460 DOI: 10.1042/bsr20203850] [Citation(s) in RCA: 34] [Impact Index Per Article: 8.5] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/31/2021] [Revised: 05/27/2021] [Accepted: 06/02/2021] [Indexed: 12/12/2022] Open
Abstract
The microbiome plays an important role in maintaining human health. Despite multiple factors being attributed to the shaping of the human microbiome, extrinsic factors such diet and use of medications including antibiotics appear to dominate. Mucosal surfaces, particularly in the gut, are highly adapted to be able to tolerate a large population of microorganisms whilst still being able to produce a rapid and effective immune response against infection. The intestinal microbiome is not functionally independent from the host mucosa and can, through presentation of microbe-associated molecular patterns (MAMPs) and generation of microbe-derived metabolites, fundamentally influence mucosal barrier integrity and modulate host immunity. In a healthy gut there is an abundance of beneficial bacteria that help to preserve intestinal homoeostasis, promote protective immune responses, and limit excessive inflammation. The importance of the microbiome is further highlighted during dysbiosis where a loss of this finely balanced microbial population can lead to mucosal barrier dysfunction, aberrant immune responses, and chronic inflammation that increases the risk of disease development. Improvements in our understanding of the microbiome are providing opportunities to harness members of a healthy microbiota to help reverse dysbiosis, reduce inflammation, and ultimately prevent disease progression.
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Qiu XQ, Cao KF, Zhang XF, Tong CY, Ma HL, Xu HM, Ma Y, Zou Z, Zhang XL, Li RQ. Defending the homeland: microbiome molecules provide protection to their vertebrate hosts. Future Microbiol 2020; 15:1697-1712. [PMID: 33350865 DOI: 10.2217/fmb-2020-0008] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/05/2023] Open
Abstract
Aim: The resident bacterial microbiome may shape and protect the health of vertebrate host. An array of molecules secreted by microbiome may contribute to the ecological stability of the microbiome itself. Material & methods: ELISA, radioactivity, immunofluorescence and cytokines measurements were used to observe the bioactivity and stability of colicin Ia level in oviparous and viviparous animal circulation. Results: Colicin Ia, a protein antimicrobial produced by Escherichia coli, is not present in animals at birth, but increases in concentration with the establishment of a stable gut microbiome and drops when the microbiome is experimentally disrupted. Colicin introduced in vivo is transported to tissues at concentrations able to prevent or eliminate bacterial infection. Conclusion: Our findings suggest an unexpected benefit provided by the presence of a resident microbiome in the form of active, circulating, bacterially-synthesized antimicrobial molecules.
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Affiliation(s)
- Xiao-Qing Qiu
- Laboratory of Biomembrane & Membrane Protein, West China Hospital, Sichuan University, Chengdu, 610041, China
| | - Ke-Fu Cao
- Laboratory of Biomembrane & Membrane Protein, West China Hospital, Sichuan University, Chengdu, 610041, China
| | - Xiao-Feng Zhang
- Laboratory of Biomembrane & Membrane Protein, West China Hospital, Sichuan University, Chengdu, 610041, China
| | - Chong-Yi Tong
- Laboratory of Biomembrane & Membrane Protein, West China Hospital, Sichuan University, Chengdu, 610041, China
| | - Hong-Lung Ma
- Laboratory of Biomembrane & Membrane Protein, West China Hospital, Sichuan University, Chengdu, 610041, China
| | - Hui-Min Xu
- Laboratory of Biomembrane & Membrane Protein, West China Hospital, Sichuan University, Chengdu, 610041, China
| | - Yue Ma
- National Center for Antimicrobial Resistance, National Institute of Food & Drug Inspection, Beijing, 100050, China
| | - Zhen Zou
- Department of Biochemistry & Molecular Biology, Peking Union Medical College, Tsinghua University, Beijing, 100005, China
| | - Xiang-Li Zhang
- Laboratory of Biomembrane & Membrane Protein, West China Hospital, Sichuan University, Chengdu, 610041, China
| | - Rong-Qi Li
- Laboratory of Biomembrane & Membrane Protein, West China Hospital, Sichuan University, Chengdu, 610041, China
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Akobeng AK, Singh P, Kumar M, Al Khodor S. Role of the gut microbiota in the pathogenesis of coeliac disease and potential therapeutic implications. Eur J Nutr 2020; 59:3369-3390. [PMID: 32651763 PMCID: PMC7669811 DOI: 10.1007/s00394-020-02324-y] [Citation(s) in RCA: 41] [Impact Index Per Article: 8.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/16/2020] [Accepted: 07/01/2020] [Indexed: 12/17/2022]
Abstract
PURPOSE Although genetic predisposition and exposure to dietary gluten are considered necessary triggers for the development of coeliac disease, alterations in the gut microbial composition may also contribute towards the pathogenesis of coeliac disease. This review aims to provide an overview of the available data on the potential mechanisms through which the gut microbiota plays a role in the causation of coeliac disease and to discuss the potential therapeutic strategies that could diminish the consequences of microbial dysbiosis. METHOD A search of the literature was performed using the PubMed, Embase, and JSTOR databases; relevant articles were included. RESULTS Recent studies in patients with coeliac disease have reported an increase in the relative amounts of gram negative bacterial genera such as Bacteroides, Prevotella, and Escherichia, and reduced amounts of protective anti-inflammatory bacteria such as Bifidobacteria and Lactobacilli. Dysbiotic microbiota may lead to a dysregulated immune response that may contribute to the pathogenesis of coeliac disease. In infancy, antibiotic use and certain infant feeding practices may lead to alterations in the developing gut microbiota to influence the immune maturation process and predispose to coeliac disease. CONCLUSION The induction of the intestinal immune system and gluten intolerance may be influenced by the relative abundance of certain microbiota. Factors such as infant feeding practices, diet, antibiotics, and infections, may be involved in the development of coeliac disease due to their influence on gut microbial composition. The efficacy of potential modulators of the gut microbiota such as probiotics, prebiotics, and fecal microbial transplant as adjunctive treatments to gluten-free diet in coeliac disease is unproven and requires further investigation.
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Affiliation(s)
- Anthony K Akobeng
- Division of Gastroenterology, Hepatology, and Nutrition, Sidra Medicine, Doha, Qatar
- Weill Cornell Medicine, Cornell University, Doha, Qatar
| | - Parul Singh
- Research Department, Sidra Medicine, Doha, Qatar
| | - Manoj Kumar
- Research Department, Sidra Medicine, Doha, Qatar
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O'Connell TM. The Application of Metabolomics to Probiotic and Prebiotic Interventions in Human Clinical Studies. Metabolites 2020; 10:metabo10030120. [PMID: 32213886 PMCID: PMC7143099 DOI: 10.3390/metabo10030120] [Citation(s) in RCA: 16] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/27/2020] [Revised: 03/10/2020] [Accepted: 03/19/2020] [Indexed: 12/12/2022] Open
Abstract
There is an ever-increasing appreciation for our gut microbiota that plays a crucial role in the maintenance of health, as well as the development of disease. Probiotics are live bacteria that are consumed to increase the population of beneficial bacteria and prebiotics are dietary substrates intended to promote the propagation of beneficial bacteria. In order to optimize the use of probiotics and prebiotics, a more complete biochemical understanding of the impact that these treatments have on the community and functioning of the gut microbiota is required. Nucleic acid sequencing methods can provide highly detailed information on the composition of the microbial communities but provide less information on the actual function. As bacteria impart much of their influence on the host through the production of metabolites, there is much to be learned by the application of metabolomics. The focus of this review is on the use of metabolomics in the study of probiotic and prebiotic treatments in the context of human clinical trials. Assessment of the current state of this research will help guide the design of future studies to further elucidate the biochemical mechanism by which probiotics and prebiotics function and pave the way toward more personalized applications.
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Affiliation(s)
- Thomas M O'Connell
- Department of Otolaryngology-Head & Neck Surgery, Indiana University School of Medicine, Indianapolis, IN 46202, USA
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12
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Cabrera-Perez J, Badovinac VP, Griffith TS. Enteric immunity, the gut microbiome, and sepsis: Rethinking the germ theory of disease. Exp Biol Med (Maywood) 2016; 242:127-139. [PMID: 27633573 DOI: 10.1177/1535370216669610] [Citation(s) in RCA: 47] [Impact Index Per Article: 5.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/15/2022] Open
Abstract
Sepsis is a poorly understood syndrome of systemic inflammation responsible for hundreds of thousands of deaths every year. The integrity of the gut epithelium and competence of adaptive immune responses are notoriously compromised during sepsis, and the prevalent assumption in the scientific and medical community is that intestinal commensals have a detrimental role in the systemic inflammation and susceptibility to nosocomial infections seen in critically ill, septic patients. However, breakthroughs in the last decade provide strong credence to the idea that our mucosal microbiome plays an essential role in adaptive immunity, where a human host and its prokaryotic colonists seem to exist in a carefully negotiated armistice with compromises and benefits that go both ways. In this review, we re-examine the notion that intestinal contents are the driving force of critical illness. An overview of the interaction between the microbiome and the immune system is provided, with a special focus on the impact of commensals in priming and the careful balance between normal intestinal flora and pathogenic organisms residing in the gut microbiome. Based on the data in hand, we hypothesize that sepsis induces imbalances in microbial populations residing in the gut, along with compromises in epithelial integrity. As a result, normal antigen sampling becomes impaired, and proliferative cues are intermixed with inhibitory signals. This situates the microbiome, the gut, and its complex immune network of cells and bacteria, at the center of aberrant immune responses during and after sepsis.
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Affiliation(s)
- Javier Cabrera-Perez
- 1 Microbiology, Immunology, and Cancer Biology Graduate Program, University of Minnesota Medical School, Minneapolis, MN 55455, USA.,2 Medical Scientist Training Program, University of Minnesota Medical School, Minneapolis, MN 55455, USA
| | - Vladimir P Badovinac
- 3 Department of Pathology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.,4 Interdisciplinary Program in Immunology, University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA
| | - Thomas S Griffith
- 1 Microbiology, Immunology, and Cancer Biology Graduate Program, University of Minnesota Medical School, Minneapolis, MN 55455, USA.,5 Department of Urology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.,6 Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.,7 Masonic Cancer Center, University of Minnesota Medical School, Minneapolis, MN 55455, USA.,8 Minneapolis VA Health Care System, Minneapolis, MN 55417, USA
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13
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Cenit MC, Codoñer-Franch P, Sanz Y. Gut Microbiota and Risk of Developing Celiac Disease. J Clin Gastroenterol 2016; 50 Suppl 2, Proceedings from the 8th Probiotics, Prebiotics & New Foods for Microbiota and Human Health meeting held in Rome, Italy on September 13-15, 2015:S148-S152. [PMID: 27741161 DOI: 10.1097/mcg.0000000000000688] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Gut microbiota shapes the development of the mucosal immune system and may provide protection against immune-mediated diseases. Celiac disease (CD) is a chronic inflammatory condition triggered by dietary gluten proteins, recently associated with gut microbiota alterations in cross-sectional studies comparing patients and controls. Whether or not these differences are causally related to the disease has yet to be elucidated, but evaluation of specific bacteria isolated from CD patients in experimental models suggests that they can promote an adverse response to dietary gluten, whereas other commensal bacteria can be protective. Genetic and environmental factors associated with increased CD risk have also been linked to shifts in the gut microbiota composition in infants early in life. Epigenetic mechanisms also seem to play an important role in modulating gut microbiota composition and function and, theoretically, could also influence CD risk. Here, we review the current knowledge on how host genetics, environmental factors, and epigenetic modifications could modulate gut microbiota functionality and how this may influence CD risk. Greater understanding of the role of this triad in CD onset and pathogenesis will be valuable in designing proof-of concept interventions in the gut ecosystem, with a view to improving CD management.
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Affiliation(s)
- Maria C Cenit
- *Microbial Ecology, Nutrition & Health Research Unit, Institute of Agrochemistry and Food Technology, National Research Council (IATA-CSIC) †Department of Pediatrics, Dr Peset University Hospital ‡Deparment of Pediatrics, Obstetrics and Gynecology, University of Valencia, Valencia, Spain
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14
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Verdu EF, Galipeau HJ, Jabri B. Novel players in coeliac disease pathogenesis: role of the gut microbiota. Nat Rev Gastroenterol Hepatol 2015; 12:497-506. [PMID: 26055247 PMCID: PMC5102016 DOI: 10.1038/nrgastro.2015.90] [Citation(s) in RCA: 143] [Impact Index Per Article: 14.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Several studies point towards alteration in gut microbiota composition and function in coeliac disease, some of which can precede the onset of disease and/or persist when patients are on a gluten-free diet. Evidence also exists that the gut microbiota might promote or reduce coeliac-disease-associated immunopathology. However, additional studies are required in humans and in mice (using gnotobiotic technology) to determine cause-effect relationships and to identify agents for modulating the gut microbiota as a therapeutic or preventative approach for coeliac disease. In this Review, we summarize the current evidence for altered gut microbiota composition in coeliac disease and discuss how the interplay between host genetics, environmental factors and the intestinal microbiota might contribute to its pathogenesis. Moreover, we highlight the importance of utilizing animal models and long-term clinical studies to gain insight into the mechanisms through which host-microbial interactions can influence host responses to gluten.
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15
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Gaudreau MC, Johnson BM, Gudi R, Al-Gadban MM, Vasu C. Gender bias in lupus: does immune response initiated in the gut mucosa have a role? Clin Exp Immunol 2015; 180:393-407. [PMID: 25603723 DOI: 10.1111/cei.12587] [Citation(s) in RCA: 30] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 01/11/2015] [Indexed: 12/28/2022] Open
Abstract
The risk of developing systemic lupus erythematosus (SLE) is approximately nine times higher among women compared to men. However, very little is understood concerning the underlying mechanisms that contribute to this gender bias. Further, whether there is a link between immune response initiated in the gut mucosa, the progression of SLE and the associated gender bias has never been investigated. In this report, we show a potential link between the immune response of the gut mucosa and SLE and the gender bias of lupus for the first time, to our knowledge. Both plasma cell- and gut-imprinted- α4β7 T cell frequencies were significantly higher in the spleen and gut mucosa of female (SWR × NZB)F1 (SNF1 ) mice compared to that of their male counterparts. Importantly, female SNF1 mice not only showed profoundly higher CD45(+) immune cell densities, but also carried large numbers of interleukin (IL)-17-, IL-22- and IL-9-producing cells in the lamina propria (LP) compared to their male counterparts. Intestinal mucosa of female SNF1 mice expressed higher levels of a large array of proinflammatory molecules, including type 1 interferons and Toll-like receptors 7 and 8 (TLR-7 and TLR-8), even before puberty. Our work, therefore, indicates that the gut immune system may play a role in the initiation and progression of disease in SLE and the associated gender bias.
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Affiliation(s)
- M-C Gaudreau
- Departments of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA
| | - B M Johnson
- Departments of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA
| | - R Gudi
- Departments of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA
| | - M M Al-Gadban
- Departments of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA
| | - C Vasu
- Departments of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA.,Departments of Surgery, College of Medicine, Medical University of South Carolina, Charleston, SC, USA
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Perna canaliculus (Green-Lipped Mussel): Bioactive Components and Therapeutic Evaluation for Chronic Health Conditions. PROGRESS IN DRUG RESEARCH 2015; 70:91-132. [DOI: 10.1007/978-3-0348-0927-6_3] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
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17
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Thoene-Reineke C, Fischer A, Friese C, Briesemeister D, Göbel UB, Kammertoens T, Bereswill S, Heimesaat MM. Composition of intestinal microbiota in immune-deficient mice kept in three different housing conditions. PLoS One 2014; 9:e113406. [PMID: 25401702 PMCID: PMC4234647 DOI: 10.1371/journal.pone.0113406] [Citation(s) in RCA: 37] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/29/2014] [Accepted: 10/23/2014] [Indexed: 01/01/2023] Open
Abstract
BACKGROUND Abundance of commensals constituting the intestinal microbiota (IM) affects the immune system and predisposes to a variety of diseases, including intestinal infections, cancer, inflammatory and metabolic disorders. Housing conditions determine the IM and can hence influence the immune system. We analyzed how both variables affect the IM of four immune-compromized mouse lines kept under different housing conditions. METHODOLOGY/PRINCIPAL FINDINGS We investigated the IM composition in mice by quantitative 16S rRNA RT-PCR analysis of the main fecal bacterial groups (Enterobacteriaceae, enterococci, lactobacilli, bifidobacteria, Bacteroides/Prevotella (BP) spp., Clostridium leptum and coccoides groups). Mice were homozygous (HO) or heterozygous (HE) for a targeted inactivating mutation of either the IFN-γ Receptor (R), IFN-γ, Rag1 or IL-4 genes. Overall, differences in IM composition were subtle. However, in the SPF-barrier, total eubacterial loads were higher in Rag1 HE versus Rag1 HO mice as well as in IFN-γR HE versus IFN-γR HO and WT animals. Although absent in WT mice, bifidobacterial loads were higher in HO and HE IFN-γ and Rag1 as well as IL-4 HO mice. Furthermore, BP was slightly lower in HO and HE IFN-γR and IFN-γ mice as well as in IL-4 HO mice as compared to WT controls. Interestingly, IM compositions were comparable in WT mice when kept in individual ventilated cages (IVC) or open cages (OC). IFN-γ HO and HE mice, however, had higher enterobacteria and BP loads, but lacked bifidobacteria when kept in OC versus IVC, as was the case in HO and HE Rag1 mice. In addition, Rag1 HO mice harbored higher clostridial loads when housed in OC as compared to IVC. Unexpectedly, lactobacilli levels were higher in IFN-γR mice when kept in OC versus IVC. CONCLUSION/SIGNIFICANCE Housing-dependent and immune-deficiency mediated changes in intestinal microbiota composition were rather subtle but may nevertheless impact immunopathology in experimental models.
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Affiliation(s)
- Christa Thoene-Reineke
- Forschungseinrichtung für Experimentelle Medizin, Charité - University Medicine Berlin, Berlin, Germany
| | - André Fischer
- Department of Microbiology and Hygiene, Charité - University Medicine Berlin, Berlin, Germany
| | - Christian Friese
- Department of Immunology, Charité - University Medicine Berlin, Berlin, Germany
| | - Dana Briesemeister
- Department of Immunology, Charité - University Medicine Berlin, Berlin, Germany
| | - Ulf B. Göbel
- Department of Microbiology and Hygiene, Charité - University Medicine Berlin, Berlin, Germany
| | - Thomas Kammertoens
- Department of Immunology, Charité - University Medicine Berlin, Berlin, Germany
| | - Stefan Bereswill
- Department of Microbiology and Hygiene, Charité - University Medicine Berlin, Berlin, Germany
| | - Markus M. Heimesaat
- Department of Microbiology and Hygiene, Charité - University Medicine Berlin, Berlin, Germany
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Zhong W, Zhou Z. Alterations of the gut microbiome and metabolome in alcoholic liver disease. World J Gastrointest Pathophysiol 2014; 5:514-522. [PMID: 25400995 PMCID: PMC4231516 DOI: 10.4291/wjgp.v5.i4.514] [Citation(s) in RCA: 49] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/24/2014] [Revised: 07/01/2014] [Accepted: 09/10/2014] [Indexed: 02/06/2023] Open
Abstract
Alcohol consumption is one of the leading causes of liver diseases and liver-related death worldwide. The gut is a habitat for billions of microorganisms which promotes metabolism and digestion in their symbiotic relationship with the host. Alterations of gut microbiome by alcohol consumption are referred to bacterial overgrowth, release of bacteria-derived products, and/or changed microbiota equilibrium. Alcohol consumption also perturbs the function of gastrointestinal mucosa and elicits a pathophysiological condition. These adverse effects caused by alcohol may ultimately result in a broad change of gastrointestinal luminal metabolites such as bile acids, short chain fatty acids, and branched chain amino acids. Gut microbiota alterations, metabolic changes produced in a dysbiotic intestinal environment, and the host factors are all critical contributors to the development and progression of alcoholic liver disease. This review summarizes recent findings of how alcohol-induced alterations of gut microbiota and metabolome, and discusses the mechanistic link between gastrointestinal dyshomeostasis and alcoholic liver injury.
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Petkau K, Parsons BD, Duggal A, Foley E. A deregulated intestinal cell cycle program disrupts tissue homeostasis without affecting longevity in Drosophila. J Biol Chem 2014; 289:28719-29. [PMID: 25170078 DOI: 10.1074/jbc.m114.578708] [Citation(s) in RCA: 34] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/22/2023] Open
Abstract
Recent studies illuminate a complex relationship between the control of stem cell division and intestinal tissue organization in the model system Drosophila melanogaster. Host and microbial signals drive intestinal proliferation to maintain an effective epithelial barrier. Although it is widely assumed that proliferation induces dysplasia and shortens the life span of the host, the phenotypic consequences of deregulated intestinal proliferation for an otherwise healthy host remain unexplored. To address this question, we genetically isolated and manipulated the cell cycle programs of adult stem cells and enterocytes. Our studies revealed that cell cycle alterations led to extensive cell death and morphological disruptions. Despite the extensive tissue damage, we did not observe an impact on longevity, suggesting a remarkable degree of plasticity in intestinal function.
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Affiliation(s)
- Kristina Petkau
- From the Department of Medical Microbiology and Immunology, Institute of Virology, University of Alberta, Edmonton, Alberta T6G 2S2, Canada
| | - Brendon D Parsons
- From the Department of Medical Microbiology and Immunology, Institute of Virology, University of Alberta, Edmonton, Alberta T6G 2S2, Canada
| | - Aashna Duggal
- From the Department of Medical Microbiology and Immunology, Institute of Virology, University of Alberta, Edmonton, Alberta T6G 2S2, Canada
| | - Edan Foley
- From the Department of Medical Microbiology and Immunology, Institute of Virology, University of Alberta, Edmonton, Alberta T6G 2S2, Canada
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Arthritis susceptibility and the gut microbiome. FEBS Lett 2014; 588:4244-9. [PMID: 24873878 DOI: 10.1016/j.febslet.2014.05.034] [Citation(s) in RCA: 86] [Impact Index Per Article: 7.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/12/2014] [Revised: 05/16/2014] [Accepted: 05/19/2014] [Indexed: 01/11/2023]
Abstract
Rheumatoid arthritis (RA) is an autoimmune disease with unknown etiology though both genetic and environmental factors have been suggested to be involved in its pathogenesis. While infections and other environmental factors (e.g. smoking) have been studied extensively and show some association, a direct link between all the factors has been difficult to prove. With the recent advances in technology, it has become possible to sequence the commensals that are residing in our gut. The gut microbiome may provide the missing link to this puzzle and help solve the mystery of many leaky gut syndromes. The gut commensals are involved in maintaining host immune homeostasis and function suggesting that they might be critical in altering the immune system, which leads to autoimmune diseases like RA. Mouse models support the role of the gut microbiota in predisposition to RA. If that is true, the power of gut-derived commensal can be harnessed to our benefit by generating a biomarker profile along with genetic factors to define individuals at risk and by altering the gut microbial composition using various means.
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Ahmer BMM. In this issue of Gut Microbes. Gut Microbes 2014; 5:83-5. [PMID: 24468723 PMCID: PMC4049943 DOI: 10.4161/gmic.28007] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/03/2023] Open
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