Abstract
BackgroundIntegrin beta-5 (ITGB5) and mucin 13 (MUC13) genes are highly expressed on the apical surface of intestinal epithelia and are thought to be candidate genes for controlling the expression of the receptor for enterotoxigenic Escherichia coli (ETEC) F4ac. Human MUC13 protein has an expected role in protecting intestinal mucosal surfaces and porcine ITGB5 is a newly identified potential receptor for ETEC F4ac.Methodology/Principal FindingsTo test the hypothesis that ITGB5 and MUC13 both play key roles in protection of the intestinal mucosa against pathogenic bacterium, porcine intestinal epithelial cells (IPEC-J2) were transfected with ITGB5-targeting, MUC13-targeting or negative control small interfering RNA (siRNA), respectively. Firstly, we measured mRNA expression levels of mucin genes (MUC4, MUC20), pro-inflammatory genes (IL8, IL1A, IL6, CXCL2), anti-inflammatory mediator SLPI, and PLAU after RNAi treatments with and without ETEC infection. Secondly, we compared the adhesions of ETEC to the pre- and post-knockdown IPEC-J2 cells of ITGB5 and MUC13, respectively. We found that ITGB5 and MUC13 knockdown both had small but significant effects in attenuating the inflammation induced by ETEC infection, and both increased bacterial adhesion in response to F4ac ETEC exposure.Conclusions/SignificanceOur current study first reported that ITGB5 and MUC13 are important adhesion molecules of mucosal epithelial signaling in response to Escherichia coli in pigs. These data suggest that both ITGB5 and MUC13 play key roles in defending the attachment and adhesion of ETEC to porcine jejunal cells and in maintaining epithelial barrier and immunity function.
Highlights
Enterotoxigenic Escherichia coli (ETEC) is recognized as a common cause of diarrhoea in humans and swine, their adherence to intestinal cells is mediated by proteinaceous, species-specific colonization factors [1]
The results indicated that mRNA expression of mucin 13 (MUC13) was significantly suppressed by the MUC13-targeting small interfering RNA (siRNA) (Fold-change = 23.48, P,0.001)
We primarily identified the effects of deficiency of MUC13 or Integrin beta-5 (ITGB5) in porcine intestinal cells upon F4ac enterotoxigenic Escherichia coli (ETEC) infection and their mucosal immunogenicity
Summary
Enterotoxigenic Escherichia coli (ETEC) is recognized as a common cause of diarrhoea in humans and swine, their adherence to intestinal cells is mediated by proteinaceous, species-specific colonization factors [1]. Besides action as a physical barrier limiting access of microbes and toxins to the underlying tissues, the contiguous lining intestinal mucosal epithelial cells secrete long filamentous cell-surface mucins which are a major constituent of the mucus barrier [12,13]. Integrin beta-5 (ITGB5) and mucin 13 (MUC13) genes are highly expressed on the apical surface of intestinal epithelia and are thought to be candidate genes for controlling the expression of the receptor for enterotoxigenic Escherichia coli (ETEC) F4ac. Human MUC13 protein has an expected role in protecting intestinal mucosal surfaces and porcine ITGB5 is a newly identified potential receptor for ETEC F4ac
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