Abstract
BackgroundThe epithelial barrier dysfunction plays a critical role in the pathogenesis of a broad array of immune diseases. Alix protein is involved in the endolysosome system. This study aims to elucidate the role of Alix in the maintenance of epithelial barrier function.ResultsThe results showed that Alix was detected in T84 cells at both mRNA and protein levels. Exposure to Staphylococcal enterotoxin B (SEB) markedly suppressed the expression of Alix in T84 cells, which could be blocked by knocking down the Toll like receptor 2. The exposure to SEB did not affect the TER, but markedly increased the permeability of T84 monolayers to OVA; the OVA passing through T84 monolayers still preserved the antigenicity manifesting inducing antigen specific T cells proliferation.ConclusionsAlix protein plays a critical role in the maintenance of the barrier function of T84 monolayers.
Highlights
The epithelial barrier dysfunction plays a critical role in the pathogenesis of a broad array of immune diseases
Exposure to Staphylococcal enterotoxin B (SEB) suppresses the expression of Alix in T84 monolayers In the first attempt, we assessed the expression of Alix in T84 cells
The results of qRT-PCR and Western blotting showed that Alix was detected in T84 cells
Summary
The epithelial barrier dysfunction plays a critical role in the pathogenesis of a broad array of immune diseases. The epithelial barrier dysfunction is recognized in a number of body disorders, such as intestinal allergy [1], inflammatory bowel diseases [2] and asthma [3]. How the microbial products passing through the epithelial barrier to arrive the deep part of tissue is elusive. The dysfunction of epithelial barrier manifests increases in the permeability to macromolecular molecules, such as protein antigens. Recent reports indicate that there are a number of factors can affect the endolysosome systems to enhance the epithelial barrier permeability [5,6,7]; the causative factors include microbial products, such as cholera toxin [5] and SEB [8].
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