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Infect. Immun. doi:10.1128/IAI.01446-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

INTERLEUKIN 12 DRIVES TH1 SIGNALING PATHWAY IN HELICOBACTER PYLORI-INFECTED HUMAN GASTRIC MUCOSA

Dipartimento di Medicina Sperimentale e Clinica, Università di Catanzaro "Magna Graecia", Catanzaro, and Dipartimento di Medicina Interna, Università di Roma "Tor Vergata", Rome, Italy

^* To whom correspondence should be addressed. Email: luzza{at}unicz.it.

	Abstract

This study examines mechanisms that regulate T helper lymphocyte (Th) 1 commitment in Helicobacter pylori-infected human gastric mucosa. Interferon (IFN)-, interleukin (IL)-4, and IL-12 were measured in total extracts of gastric biopsies taken from H. pylori-infected and uninfected patients by enzyme linked immunosorbent assay. STAT4, STAT6, and T-bet were examined in total proteins extracted from gastric biopsies by Western blotting. Finally, the effect of a neutralizing IL-12 antibody on the expression of Th1 transcription factors and levels of IFN- was examined in organ cultures of H. pylori-infected biopsies. Increased levels of IFN- and IL-12 were found in gastric biopsy samples of H. pylori-infected patients compared to uninfected patients. Accordingly, H. pylori-infected biopsies exhibited high expression of phosphorylated STAT4 and T-bet. Higher levels of IFN- and expression of Th1 transcription factors were associated with higher infiltration of mononuclear cells in the gastric mucosa. By contrast, production of IL-4 and expression of phosphorylated STAT6 were not associated with the intensity of mononuclear cell infiltration. In ex vivo organ cultures of H. pylori-infected biopsies, neutralization of endogenous IL-12 down-regulated the expression of p-Stat4 and T-bet and reduced IFN- production. Data indicate that IL-12 contributes to the Th1 cell commitment in H. pylori-infected human gastric mucosa.