Roseburia intestinalis inhibits interleukin‑17 excretion and promotes regulatory T cells differentiation in colitis

Abstract

Roseburia intestinalis (R. intestinalis) is one of the dominant intestinal bacterial microbiota and is decreased in patients with inflammatory bowel disease (IBD). It helps protect colonic mucosa against the development of inflammation and subsequent IBD, however its underlying mechanisms are unclear. The aim of the present study was to evaluate the anti-inflammatory properties of R. intestinalis in vitro and in an animal model of IBD. The effects of R. intestinalis on disease activity index (DAI) scores, intestinal pathology, the expression of interleukin (IL)-17 and the frequency of CD4+CD25+Foxp3+ regulatory T cells (Treg) were evaluated in vivo in a model of 2,4,6-trinitrobenzenesulfonic acid solution (TNBS)-induced colitis. Compared with the control group, TNBS-treated mice had significantly higher secretion of IL-17, higher DAI scores, a lower ratio of Treg, reduced colon lengths and higher histological scores for colon inflammation. The administration of R. intestinalis significantly downregulated the expression of IL-17, increased the ratio of Treg and ameliorated the high DAI scores and the pathological signs of inflammation in the colon compared with mice treated with TNBS alone. Gene expression profiling was also used to detect the expression of IL-17 in human IBD and healthy control specimens. To extend these findings to an in vitro model of inflammation the human colon epithelial cell line NCM460 was stimulated with lipopolysaccharide (LPS) to induce inflammation and co-cultured with R. intestinalis and changes in IL-17 expression were evaluated. R. intestinalis inhibited the LPS-induced secretion of IL-17 by NCM460 cells. In conclusion, these results demonstrate that R. intestinalis inhibits IL-17 secretion and promotes Treg differentiation in colitis, suggesting that R. intestinalis could be of potential use in the treatment of IBD.

Indole-3-carbinol prevents colitis and associated microbial dysbiosis in an IL-22–dependent manner

“…led to increased butyrate production and enhancement in the intestinal epithelial barrier integrity (59). In addition, a recent report shows how R. intestinalis is able to prevent IL-17 secretion and increase Treg differentiation in TNBS-induced colitis (60). There are many reports showing that butyrate is effective at alleviating the burdens inflicted by colitis, particularly through mechanisms that include increases in antimicrobial peptides (AMPs) and mucus production (61)(62)(63)(64).…”

Development of an Index Score for Intestinal Inflammation-Associated Dysbiosis Using Real-World Stool Test Results

“…We found that F. prausnitzii was negatively associated with fecal calprotectin, EPX, and IgA in the current study. The Roseburia genus [23,[30][31][32][33] or specific species (e.g., Roseburia intestinalis and Roseburia hominis) [34,35] were significantly decreased in patients with IBD. In our analysis, Roseburia spp.…”

Demystifying the manipulation of host immunity, metabolism, and extraintestinal tumors by the gut microbiome

“…27 Indeed, Roseburia intestinalis (R. intestinalis), a typical member of Clostridia, appears to be of great importance for increasing Treg cells in a colitis mouse model by reinforcing the secretion of thymic stromal lymphopoietin and TGF-β. 12,114 Attractively, flagellin, an effective modulator and crucial structure of R. intestinalis, exerts anti-inflammatory effects via activating p38-STAT1 to induce lncRNA (HIF1A-AS2) expression. 250 Nevertheless, the pleiotropic effects of R. intestinalis on host immunity have been demonstrated, as oral supplementation with R. intestinalis elicits anti-human β2-glycoprotein I autoantibodies and autoimmune pathologies in antiphospholipid syndromesusceptible mice.…”

“…The gastrointestinal tract confers a natural anaerobic environment conducive to colonization. 9 Reciprocally, the gut microbiome exerts important effects on host physiology, including controlling post-translational modifications of the host proteome, 10 stimulating immune system development and homeostasis, 11,12 maintaining intestinal barrier integrity, 13 reaping inaccessible nutrients from the diet, 14 synthesizing certain essential vitamins and neurotransmitters, 15 modulating neurobehavioral properties, 16,17 endocrine functions 18 and bone density, 19 and even participating in drug biotransformation. 20,21 Multiple factors can lead to a loss of beneficial microbes and a reduction in microbial diversity, ultimately triggering gut dysbiosis (microbial imbalance or maladaptation).…”