Diallyl sulfide pretreatment protects against DSS-induced colitis by reshaping the gut microbiota and enhancing microbiota-associated tryptophan metabolism.

Authors

Xiaoyu Wan, Yuanyu Wu, Yanan Sun, Yuxuan Liu, Guoliang Jia

Published in

Journal of ethnopharmacology. Pages 122388. Sep 12, 2026. Epub Sep 12, 2026.

Abstract

Allium sativum L. has a long-standing use in traditional medicine for gastrointestinal disorders. Diallyl sulfide (DAS), a key organosulfur compound derived from garlic, exhibits anti-inflammatory activity; however, its specific role in colitis and the underlying microbiota-metabolite mechanisms remain unresolved.
Colitis was induced in mice using DSS following DAS pretreatment. Disease severity, intestinal barrier integrity, inflammation, gut microbiota composition, tryptophan metabolites, AhR signaling, colonic IL-22 levels, and STAT3 phosphorylation were evaluated. Fecal microbiota transplantation (FMT), IPA/IAld supplementation, parallel pharmacodynamic comparisons, and AhR blockade with CH223191 were executed to explore the microbiota-metabolite-host signaling axis.
DAS pretreatment conferred protection against DSS-induced colitis, evidenced by reduced disease activity, preserved colon length, improved histological injury, suppressed inflammatory responses, and restored tight-junction proteins. DAS modified the gut microbiota and elevated local intestinal levels of IPA and IAld. FMT and IPA/IAld supplementation partially recapitulated the protective phenotype associated with DAS, while combined supplementation of IPA + IAld yielded broader protective effects, nearing the protective outcomes provided by DAS. AhR blockade via CH223191 diminished DAS-mediated protection, characterized by decreases in AhR and Cyp1a1 expression, colonic IL-22 levels, and the p-STAT3/STAT3 ratio.
DAS pretreatment offers prophylactic protection against DSS-induced colitis by altering the gut microbiota and enhancing local indole-producing tryptophan metabolism, effects mediated at least in part by the AhR/IL-22/STAT3 pathway.

PMID:
42731716
Bibliographic data and abstract were imported from PubMed on 13 Sep 2026.

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