Streptococcus infantarius and colonic cancer: Identification and purification of cell wall proteins putatively involved in colorectal inflammation and carcinogenesis in rats

Streptococcus bovis/gallolyticus Induce the Development of Colorectal Cancer

“…Therefore, this study suggests that S. bovis/gallolyticus bacteria act as potential promoters of early preneoplastic lesions in the colon of rats, and their cell wall proteins are more potent inducers of neoplastic transformation than the intact bacteria. This study also revealed that the development of colonic adenomas increased remarkably in 50% of the tested rats and the expression level of proliferation markers, the polyamine content and proliferating cell nuclear antigen was also increased (Biarc et al, 2004;Ellmerich et al, 2000a;Nguyen et al, 2006). This provided extra evidence that S. bovis/gallolyticus acts more likely as promoter/propagator of colorectal carcinoma rather than just a consequence of the tumor lesion.…”

“…Modifications in the hepatic secretion of bile salts and the production of immunoglobulins contribute towards increasing the participation of S. bovis/gallolyticus in abnormal changes in the bacterial flora of the colonic lumen which might then promote carcinogenesis of the intestinal mucosa (Beeching et al, 1985;Gupta et al, 2009). It has been suggested that alterations in local conditions and disruption of capillary channels at the site of neoplasm allowed S. bovis/gallolyticus to proliferate and gain entry into blood stream (Biarc et al, 2004;Ellmerich et al, 2000a;Nguyen et al, 2006). The local action of cytokines or of chemical mediators able to promote vasodilatation and the enhancement of capillary permeability, may support the bacterial entry at tumor sites, and increase bacterial adherence to various cells (Biarc et al, 2004;Ellmerich et al, 2000b).…”

“…In vitro experiments showed that the binding of S. bovis wall extracted antigens to various cell lines including human colonic cancer cells (Caco-2) stimulated the production of inflammatory cytokines by those cells (Biarc et al, 2004;Nguyen et al, 2006). Earlier it was found that the production of inflammatory cytokines in response to S. bovis/gallolyticus, such as TNF-α, IL-1ß and IL-6, and the chemokine IL-8, were found to contribute to the normal defense mechanisms of the host (Ellmerich et al, 2000b;Travers & Rosen, 1997) leading to the formation of nitric oxide and free radicals such as superoxide, peroxynitrites, hydroxyl radicals as well as alkylperoxy radicals (Nguyen et al, 2006;Ohshima & Bartsch, 1994).…”

“…Earlier it was found that the production of inflammatory cytokines in response to S. bovis/gallolyticus, such as TNF-α, IL-1ß and IL-6, and the chemokine IL-8, were found to contribute to the normal defense mechanisms of the host (Ellmerich et al, 2000b;Travers & Rosen, 1997) leading to the formation of nitric oxide and free radicals such as superoxide, peroxynitrites, hydroxyl radicals as well as alkylperoxy radicals (Nguyen et al, 2006;Ohshima & Bartsch, 1994). Owing to their potent mutagenicity, all these molecular species can contribute to the neoplastic processes by modifying cellular DNA.…”

“…This resembles H. pylori infection for the development of chronic inflammation in the gastric mucosa (Dixon et al, 1996); therefore, it seems that chronic infection and subsequent chronic inflammation are responsible for the maintenance and development of pre-existing neoplastic lesions (Shacter & Weitzman, 2002). Moreover, it was found that WEAs of S. bovis induced in vitro overexpression of cyclooxygenase-2 (COX-2) (Biarc et al, 2004;Nguyen et al, 2006). COX-2, via prostaglandins, promotes cellular proliferation and angiogenesis and inhibits apoptosis, thus acting as a promoter in the cancer pathway (Tafte & Ruoff, 2007).…”