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Article Abstract
Introduction: Intestinal epithelial cells produce interleukin-18 (IL-18), a key factor in promoting epithelial barrier integrity. Here, we analyzed the potential role of gut bacteria and the hypoxia-inducible factor 1α (HIF1α) pathway in regulating mucosal expression in inflammatory bowel disease (IBD).
Methods: Mucosal samples from patients with IBD ( = 760) were analyzed for bacterial composition, levels and HIF1α pathway activation. Wild-type Caco-2 and CRISPR/Cas9-engineered Caco-2--null cells were cocultured with in a "Human oxygen-Bacteria anaerobic" system and analyzed by RNA sequencing.
Results: Mucosal mRNA levels correlated positively with the abundance of mucosal-associated butyrate-producing bacteria, in particular , and with HIF1α pathway activation in patients with IBD. HIF1α-mediated expression of , either by a pharmacological agonist (dimethyloxallyl glycine) or , was abrogated in Caco-2--null cells.
Conclusion: Butyrate-producing gut bacteria like regulate mucosal expression in a HIF1α-dependent manner that may aid in mucosal healing in IBD.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10755969 | PMC |
| http://dx.doi.org/10.3389/fmicb.2023.1298304 | DOI Listing |
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