Deoxynivalenol induced inflammation and increased the adherence of entero-invasive Escherichia coli to intestinal epithelial cells via modulation of mucin and pro-inflammatory cytokine production

Abstract

Deoxynivalenol (DON) is a mycotoxin that commonly occurs in crops. It was hypothesized that DON could trigger intestinal inflammation and increase the susceptibility of intestinal epithelial cells (IECs) to pathogen infection. Accordingly, the aim of this study was to investigate the effects of DON on intestinal susceptibility to pathogen infection. Semiconfluent Caco-2 cells were exposed to DON followed by acute entero-invasive Escherichia coli (EIEC) infection. The effects of DON and EIEC contamination on mucin, cytokines and related signal transduction pathways were examined as part of the local immune system. Caco-2 cells were able to generate a rapid immune response against DON with or without EIEC post-challenge. An increase in EIEC attachment to DON-exposed cells was observed, probably in part, mediated by modulation of secretory MUC5AC mucins and membrane bound MUC4 and MUC17 mucins. Cells were also able to express and produce important mediators of inflammation, such as cytokines as a result of activation of toll-like receptors signalling cascades, modulation of nuclear factor {kappa}-light chain-enhancer of activated B cells (NK-{kappa}B) and/or mitogen-activated protein kinase (MAPK) pathways. These data indicate that DON may exert immunomodulatory effects on intestinal epithelial cells, which might thereby modify the susceptibility to bacterial infection.