ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
Intestinal epithelial AhR deletion aggravates DSS-induced colitis via lipid- and amino-acid metabolic reprogramming: integrated metabolomic-transcriptomic evidence.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundRecent studies reveal that the interaction of Aryl Hydrocarbon Receptor (AhR) signaling activation with metabolic homeostasis may significantly affect the course of IBD, and the inhibition of AhR signaling may exacerbate IBD symptoms and disrupt epithelial barrier function. However, there is no recognition of how the AhR signaling pathway affects intestinal barrier function by influencing intestinal epithelial cell metabolism.
methodsIn this study, we constructed intestinal epithelial-specific AhR knockout mice, and performed comprehensive metabolomic and transcriptomic analyses on four groups of mice (WT mice, DSS mice, AhR
resultsCompared with wild-type mice, the knockout of the AhR gene caused characteristic changes mainly in lipid metabolism and amino acid metabolism disorders, including 69 metabolites and 64 genes. Under inflammatory conditions, changes including 94 metabolites and 3062 genes were observed in the DSS group compared to wild-type mice.In addition, down-regulation of 14 metabolites and up-regulation of 11 metabolites were observed in AhR
conclusionThese genes and metabolites involved in metabolic dysregulation pathways may provide a more specific and reliable research direction to study the protective mechanisms of AhR on the intestinal epithelial barrier and provide new insights into the effects of AhR on regulating the metabolism of intestinal epithelial cells in the development of IBD.
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