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Review
. 2019 Aug 19;7(8):271.
doi: 10.3390/microorganisms7080271.

The Role of Gut Microbiota in Intestinal Inflammation with Respect to Diet and Extrinsic Stressors

Affiliations
Review

The Role of Gut Microbiota in Intestinal Inflammation with Respect to Diet and Extrinsic Stressors

Stefani Lobionda et al. Microorganisms. .

Abstract

The gut microbiota maintains a symbiotic relationship with the host and regulates several important functions including host metabolism, immunity, and intestinal barrier function. Intestinal inflammation and inflammatory bowel disease (IBD) are commonly associated with dysbiosis of the gut microbiota. Alterations in the gut microbiota and associated changes in metabolites as well as disruptions in the intestinal barrier are evidence of the relationship between the gut microbiota and intestinal inflammation. Recent studies have found that many factors may alter the gut microbiota, with the effects of diet being commonly-studied. Extrinsic stressors, including environmental stressors, antibiotic exposure, sleep disturbance, physical activity, and psychological stress, may also play important roles in altering the composition of the gut microbiota. Herein, we discuss the roles of the gut microbiota in intestinal inflammation in relation to diet and other extrinsic stressors.

Keywords: IBD; diet; dysbiosis; extrinsic stressors; gut microbiota; intestinal inflammation.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Figures

Figure 1
Figure 1
Diet alters gut microbiota associated with intestinal inflammation. Western diets containing high fat and lack of fiber changes gut microbiota population leading to a decrease of bacterial SCFAs, host AMPs, and mucus production as well as tight junction protein expression. Furthermore, it disrupts intestinal barrier, leads to bacterial translocation and increases pro-inflammatory cytokine production—resulting in intestinal inflammation. Meanwhile, prebiotic and probiotic diets provide a high fiber content, which increases the production of SCFAs, AMPs, mucus, and tight junction protein expression resulting in intact intestinal barrier and prevent from intestinal inflammation.
Figure 2
Figure 2
Alteration of gut microbiota by environmental stress impacts intestinal inflammation. Cold exposure changes the gut microbiota, which may be associated with the increase of EEC-inducing bacteria population and influence intestinal barrier function. Meanwhile, heat stress increases the population of Enterobactericeae and intestinal barrier disruption leading to intestinal inflammation. Other stressors such as high altitude, noise, pollutant and toxicant reduce anti-inflammatory gut microbiota— including Lactobacillus, Faecalibacterium, and Lachnospiraceae—increase the disruption of intestinal barrier, resulting in intestinal inflammation.
Figure 3
Figure 3
Diet and extrinsic stressors that alter the composition of gut microbiota and are associated with intestinal inflammation A western diet reduced SCFA-producing bacteria. Environmental stressors, including heat, noise, high altitude, toxicants, and pollutants decreased Faecalibacterium, Lactobacillus, and Lachnospiraceae, while increasing Enterobacteriaceae. In addition, psychological stress reduced the proportion of Lactobacillus and Lachnospiraceae. These gut microbiota alterations may decrease mucus, SCFAs, and AMPs production, as well as tight junction protein expression, resulting in intestinal inflammation.

References

    1. Backhed F., Ley R.E., Sonnenburg J.L., Peterson D.A., Gordon J.I. Host-bacterial mutualism in the human intestine. Science. 2005;307:1915–1920. doi: 10.1126/science.1104816. - DOI - PubMed
    1. Sommer F., Backhed F. The gut microbiota--masters of host development and physiology. Nat. Rev. Microbiol. 2013;11:227–238. doi: 10.1038/nrmicro2974. - DOI - PubMed
    1. Lee Y.K., Mazmanian S.K. Has the microbiota played a critical role in the evolution of the adaptive immune system? Science. 2010;330:1768–1773. doi: 10.1126/science.1195568. - DOI - PMC - PubMed
    1. Round J.L., Mazmanian S.K. The gut microbiota shapes intestinal immune responses during health and disease. Nat. Rev. Immunol. 2009;9:313–323. doi: 10.1038/nri2515. - DOI - PMC - PubMed
    1. Cani P.D. The gut microbiota manages host metabolism. Nat. Rev. Endocrinol. 2013;10:74. doi: 10.1038/nrendo.2013.240. - DOI - PubMed

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