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In the current study, the role of AhR in the regulation of an antimicrobial peptide, \u03b2\u2010defensin1 (BD\u20101) is investigated to control colitis. Human patients with ulcerative colitis (UC) and Crohn's disease (CD), and mice with three different models of colitis, express a significant decrease in the expression of BD\u20101 in colonic epithelial cells (CECs). Dietary and environmental AhR ligands induce the expression of BD\u20101 in CECs through the activation of two dioxin\u2010responsive elements (DREs) expressed on its promoter. AhR ligands attenuate colitis in wild\u2010type (WT) mice while inducing BD\u20101. However, AhR ligands fail to induce BD\u20101 and protect mice from colitis when there is an intestinal epithelial cell (IEC)\u2010specific deletion of AhR. Blocking BD1 in vivo using antibodies prevents the ability of AhR ligands to ameliorate colitis, restore dysbiosis, and attenuate colonic inflammation. The current study identifies a novel pathway involving dietary, environmental, and endogenous AhR ligands to induce the antimicrobial peptide BD\u20101 in IECs, which in turn, plays a critical role in the regulation of intestinal homeostasis.<\/jats:p>","DOI":"10.1002\/advs.202416324","type":"journal-article","created":{"date-parts":[[2025,5,24]],"date-time":"2025-05-24T00:41:19Z","timestamp":1748047279000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["AhR\u2010Dependent Induction of \u03b2\u2010Defensin 1 in Colonic Epithelial Cells Regulates Cross\u2010Talk between Gut Microbiota and Immune Response Leading to Attenuation of Colitis"],"prefix":"10.1002","volume":"12","author":[{"given":"Manikandan","family":"Palrasu","sequence":"first","affiliation":[{"name":"Department of Pathology Microbiology and Immunology University of South Carolina School of Medicine  Columbia SC 29208 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