The results showed that H. pylori increased TGFβ production and decreased CFTR and SLC26A6 expressions in SCBN cells, which depended on multiplicity of infection of H. pylori. Moreover, forskolin- and PGE2-stimulated bicarbonate secretions were markedly decreased in H. pylori-infected SCBN cells in comparison with controls. Here, TGFB1 is linked to infection.