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In a previous study, we reported that a wbpP gene mutation in Vibrio vulnificus was significantly impaired in its ability to synthesize surface capsular polysaccharide (CPS). In this study, we evaluated the functions of the V. vulnificus capsular polysaccharide on interleukin (IL)-8 production, as well as its underlying mechanisms in human intestinal epithelial cells. The CPS-defective wbpP mutant induced significantly lower levels of IL-8 production, IL-8 gene promoter activation and NF-kappaB activity in INT-407 cells than was noted with the wild-type or wbpP-complemented V. vulnificus. The expression levels of Toll-like receptor (TLR)2 mRNA and protein were also found to be lower in INT-407 cells infected with the CPS-defective wbpP mutant than in those cells infected with the wild-type or the wbpP-complemented strains. Additionally, the treatment of INT-407 cells with anti-TLR2 antibody proved to significantly block IL-8 production and NF-kappaB minimal promoter activity induced by the wild-type or the wbpP-complemented strains. Furthermore, purified V. vulnificus CPS was found to significantly induce IL-8 production and NF-kappaB activation, both of which were inhibited upon the addition of the anti-TLR2 antibody. Taken together, these results demonstrate that V. vulnificus capsular polysaccharide is involved in the induction of IL-8 production of human intestinal epithelial cells via a TLR2/NF-kappaB-dependent pathway.

Involvement of capsular polysaccharide via a TLR2/NF-κB pathway in Vibrio vulnificus-induced IL-8 secretion of human intestinal epithelial cells