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• W4380086808 abstract "<h3>Background</h3> Crohn’s disease (CD) is a chronic inflammatory disorder characterized by intestinal immune dysfunction. Multiple factors, including gut dysbiosis, are involved in the pathogenesis of CD. However, the effect of commensal bacteria on controlling the inflammatory response in individuals with CD remains unclear. <h3>Methods</h3> We detected Toll-like receptor 2 (TLR2), TLR4, and TLR5 expression in R. intestinalis-treated mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. Then, we quantified the signs of colonic inflammation, the proportion of regulatory T cells (Tregs) and the expression of thymic stromal lymphopoietin (TSLP) and transforming growth factor (TGF)-β in TLR-5-deficient (Tlr5-/-) mice, bone marrow chimera mice (generated using wild-type (WT) and Tlr5-/- mice), and anti-TSLP/anti-TGFβ-treated C57BL/6 mice with colitis induced by TNBS. In vitro, we used the lipopolysaccharide (LPS)-stimulated human intestinal epithelial cell line Caco-2 as an inflammatory colon cell model treated with or without the TLR5-siRNA intervention in the presence of R. intestinalis and incubated human monocyte-derived dendritic cells (DCs) with the supernatant of Caco-2 cells. Then, we cocultured human CD4+ T cells with the aforementioned DCs to determine the differentiation of Tregs. Additionally, samples from patients with CD were collected to analyse the correlation between TLR5/TSLP/TGFβ expression and the percentage of R. intestinalis. <h3>Results</h3> Here, we show that R. intestinalis inhibits the development of CD by increasing the differentiation of anti-inflammatory Tregs. Mechanistically, R. intestinalis stimulates TSLP production in intestinal epithelial cells (IECs) through TLR5 but not TLR2 or TLR4. TSLP produced by IECs specifically induces the secretion of IL-10 and TGFβ from DCs, which is necessary for subsequent Treg differentiation. Consequently, the depletion of TLR5 (using Tlr5-/- mice) or inhibition of TSLP (using anti-TSLP neutralizing antibodies) attenuates the protective effect of R. intestinalis on experimental colitis in mice (IDDF2023-ABS-0302 Figure 1. A proposed model illustrating the inflammation inhibitory effect of R intestinalis on colitis). Importantly, the expression of TSLP in patients with CD is positively correlated with the level of R. intestinalis. <h3>Conclusions</h3> These findings reveal the previously unknown mechanism of R. intestinalis-mediated intestinal immune regulation, which may provide the basis for new therapeutic strategies for CD." @default.
• W4380086808 created "2023-06-10" @default.
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• W4380086808 date "2023-06-01" @default.
• W4380086808 modified "2023-09-27" @default.
• W4380086808 title "IDDF2023-ABS-0302 Study on the anti-inflammatory mechanism of roseburia intestinalis including differentiation of the regulatory T cells via TLR5 on the intestinal epithelial cells in inflammatory bowel disease" @default.
• W4380086808 doi "https://doi.org/10.1136/gutjnl-2023-iddf.117" @default.
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