Observational analysis reveals alterations in transepithelial permeability and inflammatory response in epithelial cells, indicating hydrogen sulfide's regulatory role.
Abstract The intestinal epithelial barrier is essential for protecting against pathogens and toxins while permitting nutrient and water absorption. Barrier dysfunction is a hallmark of inflammatory diseases affecting the gastrointestinal (GI) tract and beyond. Hydrogen sulfide (H₂S) has emerged as a critical regulator of intestinal homeostasis. This study examines the effects of the H₂S-releasing compound 4-hydroxithiobenzamide (TBZ) on epithelial barrier integrity. While TBZ did not prevent interferon-γ and tumor necrosis factor-α (IFN/TNF)-induced epithelial cell death, it reversed cytokine-induced increases in transepithelial permeability. Interestingly, TBZ alone elevated paracellular permeability, yet normalized it under inflammatory conditions, indicating a context-dependent effect. H₂S-producing enzymes localized apically in intestinal epithelial cells, suggesting spatial regulation. Transcriptomic analysis implicated oxidative phosphorylation as a pathway mediating TBZ’s effects. These findings advance our understanding of H₂S in intestinal barrier regulation and support TBZ as a candidate therapeutic agent for conditions marked by barrier dysfunction in an inflammatory context.
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Oliveira et al. (2025) studied this question.
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