The Prevalence and Polymorphisms of Zonula Occluden Toxin Gene in Multiple Campylobacter concisus Strains Isolated from Saliva of Patients with Inflammatory Bowel Disease and Controls

Abstract

Campylobacter concisus is an oral bacterium. A number of studies detected a significantly higher prevalence of C. concisus in the intestinal tract of patients with inflammatory bowel disease (IBD) as compared to controls. The prevalence of zonula occluden toxin (zot) gene, which encodes a toxin known to increase intestinal permeability, in oral C. concisus strains is unknown. Increased intestinal permeability is a feature of IBD. A total of 56 oral C. concisus strains isolated from 19 patients with IBD and 20 controls were examined (some individuals were colonized with multiple strains). A filtration method was used for isolation of C. concisus from saliva samples. SDS-PAGE was used to define strains. PCR was used to amplify zot from C. concisus strains. Positive PCR products were sequenced and the nucleotides and amino acids were compared. Of the 56 oral C. concisus strains examined, 17 strains (30.4%) were positive for zot. The prevalence of zot-positive oral C. concisus strains was 54.5% in patients with active IBD, which was not significantly different from that in healthy controls (40%). Polymorphisms of C. concisus zot were revealed. zot808T, zot350-351AC and zotMultiple were detected only in patients with IBD, but not in healthy controls. Both zot808T and zotMultiple alleles resulted in substitution of valine at position 270, which occurred in 36.4% of patients with active IBD but not in healthy controls (P = 0.011). Furthermore, the prevalence of multiple oral C. concisus strains in patients with active IBD was significantly higher than that in healthy controls (P = 0.013). This is the first study reporting the prevalence of zot in human oral C. concisus strains and the polymorphisms of C. concisus zot gene. The data suggest that the possible role of C. concisus strains containing specific polymorphic forms of zot gene in human IBD should be investigated. © 2013 Mahendran et al.