ArticleCellular and molecular life sciences : CMLS2025
Oxysterol-mediated modulation of intestinal inflammation: insights into sex differences and GPR183 signaling.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Age and sex: dual drivers remodeling the anti-tumor immune microenvironment and shaping personalized immuno-oncology.Frontiers in immunology · 2026Review
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7 authors.
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Abstract
BACKGROUND AND
aimsOxysterols, oxidized derivatives of cholesterol, play complex roles in inflammatory processes, but their specific functions in inflammatory bowel diseases remain incompletely understood. This study investigates the roles of key oxysterols - 7α,25-dihydroxycholesterol, 25-hydroxycholesterol, 25-hydroxycholesterol-3-sulfate, and 4β-hydroxycholesterol - and potential sex differences in intestinal inflammation.
methodsWe used complementary approaches including dextran sulfate sodium-induced colitis, and ex vivo studies with colon explants, organoids, and immune cells to examine oxysterol properties. Principal component analysis was employed to analyze variance between disease and sex. In vivo administration of 7α,25-dihydroxycholesterol and NIBR189, an antagonist of its receptor GPR183, was performed to assess effects on inflammatory markers and immune cell trafficking.
resultsWe observed sex-specific differences in both basal and colitis-induced oxysterol profiles, with female mice showing greater resistance to dextran sulfate sodium-induced inflammation and distinct patterns of oxysterol metabolism. Principal component analysis highlighted a separation of samples by both treatment and sex, with dextran sulfate sodium treatment accounting for approximately 55% of variance and sex differences explaining 25%. In vitro, 25-hydroxycholesterol-3-sulfate and 7α,25-dihydroxycholesterol decreased inflammatory cytokine expression in colon explants from female mice and reduced cytokine production in THP-1-derived macrophages in a dose-dependent manner. GPR183 antagonists decreased cell activation, suggesting constitutive receptor activity. In vivo 7α,25-dihydroxycholesterol administration showed modest effects on inflammatory markers but significantly decreased immune cell counts in lymph nodes, consistent with altered immune cell trafficking.
conclusionOur findings reveal sex-specific regulation of inflammatory processes by oxysterols and highlight the therapeutic potential of targeting these pathways in inflammatory bowel diseases.
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