pylori infection should have an apparent effect in preventing virulence factor release by stressed or dying bacteria apart from its bacteriostatic or bactericidal activity. Additionally, when allitridi undergoes partial degradation in vivo or there is interference with other factors, it would still be helpful for patients because subinhibitory concentrations of allitridi

effectively suppresses the production of virulence proteins. It has been well documented that VacA plays a role in H. pylori colonization, survival (Salama et al., 2001) and epithelial damage (Telford et al., 1994), whereas CagA is associated with higher grades of gastric CAL-101 concentration mucosal inflammation, atrophic gastritis and gastric carcinoma (Hatakeyama & Higashi, 2005). Therefore, application of allitridi can be expected to decrease the probability of H. pylori infection and to prevent the incidence of H. pylori-related gastric diseases. In this study, our data indicate that the bacteriostatic mechanism of allitridi in H. pylori can

be attributed to its multitarget Navitoclax in vitro inhibitory effects. Figure 4 shows a simple model of the antibacterial mode of action of allitridi according to our results. However, it is still unclear whether this inhibitory effect is direct or indirect. The chemical structure of DATS is allyl-S-S-S-allyl (C6H10S3) (Davis, 2005). It has been suggested that garlic-derived organosulfur compounds can modify SH-containing enzymes via thiol-disulfide exchange (Pinto et al., 2006). The reaction of DATS with protein thiols is allyl-S-S-S-allyl+protein-SHprotein-S-S-allyl+allyl-S-SH. This reaction may either activate or inactivate the SH-containing protein, which is dependent on the intrinsic nature of a protein or an enzyme (Klatt selleck kinase inhibitor & Lamas, 2000). We postulate that the primary targets of allitridi are likely to

be the SH-containing proteins, and the activity variation of SH-containing protein would result in abundant changes in certain proteins. In summary, to our knowledge, the present study, for the first time, elucidates the antibacterial mode of action of allitridi at a global protein level, which provides a theoretical basis for the potential application of allitridi as a therapeutic agent against H. pylori infection. However, more clinical evaluations of the anti-H. pylori activity of allitridi are still needed. This work was supported by the National Natural Science Foundation of China (accession numbers 30770118, 3000406, 30800037, 30972775 and 30800614), the National Basic Research Program of China (973 Program 2007CB512001) and the Science Foundation of Shandong Province (accession numbers 2005GG3202087 and Y2004C03). S.L. and Y.S. contributed equally to this work. “
“During the establishment of Escherichia coli O157:H7 infection, its capacity to adhere to host intestinal epithelial cells is the critical first step in pathogenesis.