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Review
. 2020 Oct 15;8(10):1587.
doi: 10.3390/microorganisms8101587.

"V体育2025版" Gut Microbiota and Immune System Interactions

Ji Youn Yoo  1 , Maureen Groer  1 , Samia Valeria Ozorio Dutra  2 , Anujit Sarkar  1   3 , Daniel Ian McSkimming  4
Affiliations
Review

Gut Microbiota and Immune System Interactions

V体育ios版 - Ji Youn Yoo et al. Microorganisms. .

Erratum in

Abstract

Dynamic interactions between gut microbiota and a host's innate and adaptive immune systems play key roles in maintaining intestinal homeostasis and inhibiting inflammation VSports手机版. The gut microbiota metabolizes proteins and complex carbohydrates, synthesize vitamins, and produce an enormous number of metabolic products that can mediate cross-talk between gut epithelial and immune cells. As a defense mechanism, gut epithelial cells produce a mucosal barrier to segregate microbiota from host immune cells and reduce intestinal permeability. An impaired interaction between gut microbiota and the mucosal immune system can lead to an increased abundance of potentially pathogenic gram-negative bacteria and their associated metabolic changes, disrupting the epithelial barrier and increasing susceptibility to infections. Gut dysbiosis, or negative alterations in gut microbial composition, can also dysregulate immune responses, causing inflammation, oxidative stress, and insulin resistance. Over time, chronic dysbiosis and the translocation of bacteria and their metabolic products across the mucosal barrier may increase prevalence of type 2 diabetes, cardiovascular disease, inflammatory bowel disease, autoimmune disease, and a variety of cancers. In this paper, we highlight the pivotal role gut microbiota and their metabolites (short-chain fatty acids (SCFAs)) play in mucosal immunity. .

Keywords: gut dysbiosis; gut microbiota; gut microbiota metabolites; immune system; short-chain fatty acids (SCFAs). V体育安卓版.

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Conflict of interest statement

The authors declare no conflict of interest.

"V体育2025版" Figures

Figure 1
Figure 1
The interaction between microbiota-derived metabolism in the gut epithelium. (A) In the gut homeostatic condition, gut microbiota, especially butyrate-producing bacteria, converts fiber into fermentation products such as SCFAs. These SCFAs stimulate a PPAR-γ–dependent activation of mitochondrial-oxidation, thereby lowering epithelial oxygenation. SCFAs also directly bind G protein-coupled receptors (GPCRs), such as GPR41, GPR43, and GPR109A, on the surface of epithelial cells and immune cells that lead to decrease inflammation in the gut. Transport or diffusion of SCFAs into host cells results in their metabolism and/or inhibition of histone deacetylase (HDAC) activity (not shown). (B) During the gut dysbiosis, Enterobacteriaceae uses its virulence factors to trigger neutrophil transepithelial migration, which leads to a depletion of SCFA-producing bacteria, thereby lowering the luminal concentration of short-chain fatty acids such as butyrate. The consequent metabolic reprogramming of the epithelium increases the luminal bioavailability of oxygen (O2) and lactate. Arrows represent increases (red) and decreases (blue) in bacterial abundances, metabolites, and downstream effects observed in the homeostatic and dysbiotic guts.
Figure 2
Figure 2
Gut dysbiosis. Antibiotic treatment or other factors can disrupt the commensal microbial community, resulting in diminished resistance to colonization by pathogens and the outgrowth of indigenous pathobionts, such as Clostridium difficile. C. difficile can produce toxins, like TcdA and TcdB, that destroy the epithelial barrier and increase gut permeability. This toxin-mediated epithelial damage can cause systemic circulation of bacteria, which is associated with increasing systemic inflammation. Pathogen-induced gut inflammation confers a growth advantage to the pathogen through the generation of molecules such as inducible nitric oxide synthase (iNOS) by host innate immune cells leading to the release of nitrate (NO3−), which can be used as an electron acceptor by Escherichia coli to generate energy through nitrate respiration. Pathogen infection results in the conversion of pro-IL-1β into the enzymatically active mature form of IL-1β, which promotes neutrophil recruitment and pathogen eradication. Bacterial toxins stimulate the NLRP3 inflammasome, driving the proteolytic activation of caspase-1, which results in the release of mature, biologically active IL-18 and IL-1β. Arrows represent increases (red) and decreases (blue) in bacterial abundances, metabolites and downstream effects observed in the antibiotic treated dysbiotic gut.
Figure 3
Figure 3
Human gut microbial dysbiosis has a close relationship with diseases. The immune system–gut microbiota crosstalk is of sublime importance in understanding the role of dysbiosis-driven diseases in humans. Gut dysbiosis induces immune dysregulation and subsequently increase the risk of developing diseases, including inflammatory bowel disease (IBD), diabetes, obesity, cardiovascular diseases (CVDs), infectious disease, and autoimmune disease.
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