The differential transcription or metabolism of pyruvate was not at VC1844 gene level and there must be a regulation mechanism, which acts at the pyruvate point, differs between the toxigenic and nontoxigenic strains. The most CB-5083 important difference between the toxigenic and nontoxigenic strains is the presence or absence of the cholera toxin gene ctxAB. When we deleted

ctxAB from the toxigenic strains or complemented ctxAB via plasmid into the nontoxigenic strains, we did not observe the reversion of the sorbitol fermentation rate when comparing the mutants with the wild-type strains (data not shown). In the proteomic analysis, we identified two virulence-related proteins. Among them, hemolysin has a predominant role in lethality and confers V. cholerae the ability to prevent clearance and establish prolonged colonization without a requirement for cholera toxin or toxin-coregulated pili [20, 21]. V. cholerae Hcp protein is a 28-kDa secreted protein regulated coordinately with hemolysin. The expression

of both proteins has been shown to promote expression of virulence determinants in vivo and increase LD50 in the infant mouse cholera model [22, 23]. Consistent with their co-regulation relationship, both hemolysin and hcp were more abundant in the N16961 sorbitol culture profiles, suggesting that sorbitol induction and metabolism may have relationship with the regulation of the expression of virulent elements in V. cholerae. Conclusion We carried out a comparative analysis of the differences induced by sorbitol between toxigenic (sorbitol slow fermentation) and nontoxigenic BAY 1895344 mouse (sorbitol fast fermentation) V. cholerae strains. Our results suggest that the differential expression of the FIIA protein and MtlD of mannitol PTS demonstrate changes in the transportation and metabolism of sorbitol, and that pyruvate PF-02341066 solubility dmso dehydrogenase and PFL relate to the different production rate Olopatadine of the acid metabolites.

The contribution and functional mechanisms of these proteins in the V. cholerae sorbitol fermentation pathway in toxigenic and nontoxigenic strains will require further study. Acknowledgements This work was supported by the grants from the National Natural Science Foundation of China (30070041 and 30500026). Electronic supplementary material Additional file 1: The differential protein spots identified by PMF. In this table the protein spots with the differential abundance in the proteome comparisons of SJ/FJ and SN/FN in sorbitol and fructose fermentation media respectively, and their PMF identification results, were listed. (DOC 184 KB) References 1. Faruque SM, Nair GB: Molecular ecology for toxigenic Vibrio cholerae. Microbiol Immunol 2002, 46:59–66.PubMed 2. Chen F, Evins GM, Cook WL, Almeida R, Hargrett-Bean N, Wachsmuth K: Genetic diversity among toxigenic and nontoxigenic Vibrio cholerae O1 isolated from the Western hemisphere. Epidemiol Infect 1991, 107:225–233.CrossRefPubMed 3.