Adherent-invasive Escherichia coli LF82 disrupts the tight junctions of Caco-2 monolayers.

Background and study aims: Adherent invasive Escherichia coli (AIEC) are enriched in IBD (inflammatory bowel disease) patients, but the role and mechanism of AIEC in the intestinal epithelial barrier is poorly defined. We evaluated the role of the AIEC strain E. coli LF82 in vitro and investigated the role of Th17 in this process.

Material and methods: After coincubation with AIEC, the epithelial barrier integrity was monitored by epithelial resistance measurements. The permeability of the barrier was evaluated by TEER (trans-epithelial electrical resistance) and mucosal-to-serosal flux rate. The presence of interepithelial tight junction proteins ZO-1 and Claudin-1 were determined by immunofluorescence and western blot analysis. Cytokines in the cell culture supernatant were assayed by enzyme-linked immunosorbent assay (ELISA).

Results: AIEC infection decreased TEER and increased the mucosal-to-serosal flux rate of Lucifer yellow in the intestinal barrier model in a time- and dose-dependent manner. AIEC infection decreased the expression and changed the distribution of ZO-1 and claudin-1. It also induced the secretion of cytokines such as TNF-α and IL-17.

Conclusion: AIEC strain E. coli LF82 increased the permeability and disrupted the tight junctions of the intestinal epithelial barrier, revealing that AIEC plays an aggravative role in the inflammatory response.