Progress in research on interaction of intestinal microbiota and immunity
The human intestinal tract is the largest immune organ in the body and comprises cells from nonhemopoietic (epithelia, Paneth cells, goblet cells) and hemopoietic (macrophages, dendritic cells, T-cells), and have trillions of microbes collectively. The microbiota and host immune system communicate w...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Zhejiang University Press
2016-05-01
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| Series: | 浙江大学学报. 农业与生命科学版 |
| Subjects: | |
| Online Access: | https://www.academax.com/doi/10.3785/j.issn.1008-9209.2015.10.141 |
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| Summary: | The human intestinal tract is the largest immune organ in the body and comprises cells from nonhemopoietic (epithelia, Paneth cells, goblet cells) and hemopoietic (macrophages, dendritic cells, T-cells), and have trillions of microbes collectively. The microbiota and host immune system communicate with each other to mutually maintain homeostasis.Gut microbiota can have important consequences for the development of inflammatory diseases, including autoimmune diseases and allergy, and the specific mechanisms by which the gut commensals impel the development of diverse types of immune responses are beginning to be understood. Gut microbiota has been shown to direct maturation of the host immune system, to play an important role in the induction of CD4<sup>+</sup> T cell (including Th1, Th17 and Foxp3<sup>+</sup> regulatory T cell) and immunoglobulin A (IgA), and the expression of antimicrobial peptides. Intestinal colonization of altered Schaedler flora (ASF) resulted in activation and de novo generation of colonic Treg cells. Failure to activate Treg cells resulted in the induction of T helper 17 (Th17) and Th1 cell responses. Thus, microbiota colonization-induced Treg cell responses are a fundamental intrinsic mechanism to induce and maintain host-intestinal microbial T cell mutualism. Commensals are rapidly killed by macrophages, intestinal dendritic cells (DCs) can keep small numbers of live commensals for a few days, which makes DCs selectively induce IgA. The commensal-loaded DCs are confined to the mucosal immune compartment by the mesenteric lymph nodes, which assure that immune responses to gut bacteria are induced locally, without potentially damaging systemic immune responses. The production of cathelicidin related antimicrobial peptide (CRAMP) by insulin secreting β-cells was controlled by short chain fatty acids produced by the gut microbiota. Therefore, gut microbiota manipulations in non-bese diabetic (NOD) mice modulated CRAMP production and inflammation in the pancreatic islets, exposing that the gut microbiota directly shape the pancreatic immune environment and autoimmune diabetes development.There may be numerous molecules produced by gut microbes that affect these immune responses. Meanwhile, targeting gut microbiota might be an effective strategy to overcome diseases, which was proved by many experimental and clinical researches. Accordingly, if these mechanisms are fully understood, diseases can be treated with probiotics/prebiotics to regulate gut microbes. Here, this review advances our understanding of the interactions between resident microbes and the immune system, and the implications of these findings for human health. |
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| ISSN: | 1008-9209 2097-5155 |