International immunopharmacology · 2026
H2S alleviates fear condition-induced exacerbated colitis by promoting IgA production.
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Fang Fang, Xue Meng, Wang Yamin, Wang Song, Jiang Wenjun
Аннотация
INTRODUCTION: The impact of psychological stress on colitis and the alleviating effects of H2S on colitis have been partially explored. However, the effects of panic on colitis and whether H2S can mitigate colitis exacerbated by psychological stress remain unclear.
OBJECTIVES: This study aims to investigate whether fear condition exacerbates colitis and its underlying mechanisms, as well as whether H2S can alleviate colitis aggravated by psychological stress and the specific mechanisms involved.
METHODS: We conducted fear condition modeling in DSS-induced colitis mice to examine whether fear condition exacerbates colitis and whether H2S administration can alleviate the exacerbated colitis caused by fear condition. Colonic tissues from different groups of mice were subjected to RNA-seq analysis to explore potential mechanisms. Based on changes in IgA levels, we assessed alterations in IgA-coated bacteria within the gut microbiota of the different groups. Using Rag1-/- mice, we further validated the relationship between H2S, IgA, and colitis. Additionally, we knocked down AID expression in B cells to investigate whether H2S affects IgA production through AID. Finally, we tested whether H2S-mediated promotion of IgA also provides anti-infective effects in Citrobacter rodentium infection.
RESULTS: We found that H2S alleviates fear condition exacerbated colitis by promoting IgA production and modulating the gut microbiota. The promotion of IgA production by H2S in B cells is AID-dependent. Furthermore, H2S-mediated IgA enhancement also exhibits anti-infective effects.
CONCLUSION: H2S can alleviate colitis exacerbated by fear conditioning and exert anti-infective effects by promoting IgA production in B cells.
OBJECTIVES: This study aims to investigate whether fear condition exacerbates colitis and its underlying mechanisms, as well as whether H2S can alleviate colitis aggravated by psychological stress and the specific mechanisms involved.
METHODS: We conducted fear condition modeling in DSS-induced colitis mice to examine whether fear condition exacerbates colitis and whether H2S administration can alleviate the exacerbated colitis caused by fear condition. Colonic tissues from different groups of mice were subjected to RNA-seq analysis to explore potential mechanisms. Based on changes in IgA levels, we assessed alterations in IgA-coated bacteria within the gut microbiota of the different groups. Using Rag1-/- mice, we further validated the relationship between H2S, IgA, and colitis. Additionally, we knocked down AID expression in B cells to investigate whether H2S affects IgA production through AID. Finally, we tested whether H2S-mediated promotion of IgA also provides anti-infective effects in Citrobacter rodentium infection.
RESULTS: We found that H2S alleviates fear condition exacerbated colitis by promoting IgA production and modulating the gut microbiota. The promotion of IgA production by H2S in B cells is AID-dependent. Furthermore, H2S-mediated IgA enhancement also exhibits anti-infective effects.
CONCLUSION: H2S can alleviate colitis exacerbated by fear conditioning and exert anti-infective effects by promoting IgA production in B cells.