Modulation of Cytokine-Induced Intestinal Epithelial Dysfunction by Lactic Acid Bacteria

Lactic acid bacteria (LAB) contribute to intestinal barrier homeostasis. However, their role in mitigating inflammation-associated epithelial dysfunction remains insufficiently defined. This study investigated the LAB capacity to modulate cytokine-induced barrier perturbation using an in vitro human intestinal epithelial model. Differentiated HT-۲۹ monolayers were challenged with pro-inflammatory cytokines (TNF-α, IL-۱β, and IFN-γ) to induce inflammatory barrier dysfunction. Bacterial viability and epithelial adhesion were initially evaluated, followed by the assessment of cytokine responses under inflammatory conditions. The bacteria remained viable and adhered efficiently to epithelial cells, with maximal adhesion observed at an HT-۲۹: bacteria ratio of ۱:۱۰,۰۰۰. Cytokine stimulation increased inflammatory mediator levels, with ۴۸ h identified as the optimal induction period. LAB treatment was associated with lower TNF-α concentrations across tested ratios. In contrast, IL-۱β and IFN-γ responses were concentration-dependent: exposure at a ۱:۱,۰۰۰ ratio increased cytokine levels, while treatment at a ۱:۱۰,۰۰۰ ratio attenuated their production. These findings suggest dose-dependent immunomodulatory effects of LAB on cytokine-challenged intestinal epithelial cells and support their potential as therapeutic candidates for restoring epithelial barrier integrity under inflammatory stress.

کلیدواژه ها:

Lactic acid bacteria ، HT-۲۹ cell line ، TNF-&alpha ، IL-۱&beta ، IFN-& gamma