Helicobacter pylori infection of human gastric epithelial cells induces IL-8 and TNFalpha, but not TGFbeta1 mRNA.

Helicobacter pylori (Hp) infection causes gastric ulcers and gastric carcinomas. The mechanisms of these diseases are not known but Hp induction of cytokines is believed to be involved. However, the profile as well as the involvement of cytokines induced by Hp infection is less clear. In the present study, steady state levels of interleukin-8 (IL-8), tumor necrosis factor-alpha (TNFalpha) and TGFbeta1 mRNA of human gastric epithelial cell lines Kato III, AGS and NCI-87N in response to Hp infection were investigated. The cell cultures were infected with Hp for up to 18 h. Total RNA was extracted and analyzed by reverse transcription-PCR. The three cell lines tested expressed low constitutive levels of mRNA for IL-8 and TNFalpha. The mRNA levels of IL-8 quickly increased within 2 h in all three cells tested and reached a peak at 4 h following infection with Hp. In contrast, the levels of TNFalpha after Hp infection increased in only Kato III cells. The other cells, AGS and NCI-87N, responded with minimum increases after Hp infection. The TGFbeta1 mRNA was constitutively expressed in both AGS and NCI-87N cells, but Kato III cells expressed only low levels prior to infection. The Hp infection did not increase the levels of TGFbeta1 mRNA as well as TGFbeta1 secretion in all cells tested. These results indicate that the cytokine response to Hp infection differs according to the cells studied and the response may be linked somewhat to TGF levels of gastric cells.