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)-β 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-β and IL-10 production, we investigated the expression of TGF-β and IL-10 in various mammalian cell lines preincubated with H. pylori and other enteric bacteria. Results. The amount of TGF-β protein, but not IL-10, was significantly increased after stimulation with H. pylori, but other enteric bacteria did not induce TGF-β 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-β 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-β-inducing protein") that induces production of TGF-β. In view of the multiple effects of TGF-β, we conclude the TGF-β-inducing protein of H. pylori might mediate the immune response and contribute to the pathogenesis of H. pylori infection.