Preferential induction of transforming growth factor-beta production in gastric epithelial cells and monocytes by Helicobacter pylori soluble proteins

Abstract

Background. The cytokines induced by Helicobacter pylori, as well as the intricate balance of proinflammatory and anti-inflammatory cytokines, are relevant to the outcomes of H. pylori infection. Transforming growth factor (TGF)-beta and interleukin (IL)-10 are 2 vital anti-inflammatory cytokines that regulate mucosal immunity in various inflammatory and infectious diseases. Methods. To elucidate whether host-bacteria interaction can influence TGF-beta and IL-10 production, we investigated the expression of TGF-beta and IL-10 in various mammalian cell lines preincubated with H. pylori and other enteric bacteria. Results. The amount of TGF-beta protein, but not IL-10, was significantly increased after stimulation with H. pylori, but other enteric bacteria did not induce TGF-beta production. Different H. pylori strains isolated from patients with gastritis, peptic ulcer, gastric cancer and strains with cagA or vacA isogenic mutations showed similar effects on TGF-beta induction, indicating that this effect was a constitutional characteristic of H. pylori and independent of cagA and vacA status. Conclusion. The results imply the presence of a protein factor ( termed "TGF-beta-inducing protein") that induces production of TGF-beta. In view of the multiple effects of TGF-beta, we conclude the TGF-beta-inducing protein of H. pylori might mediate the immune response and contribute to the pathogenesis of H. pylori infection.