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Infection and Immunity, March 2000, p. 1189-1195, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Tumor Necrosis Factor Alpha and Interleukin 1beta Up-Regulate Gastric Mucosal Fas Antigen Expression in Helicobacter pylori Infection

JeanMarie Houghton,1,* Lisa S. Macera-Bloch,2 Lawrence Harrison,3 Kyung H. Kim,4 and Reju M. Korah5

Division of Gastroenterology1 and Division of Medical Oncology,5 Department of Medicine, Department of Microbiology and Molecular Genetics,2 and Division of Surgical Oncology, Department of Surgery,3 University of Medicine and Dentistry of New Jersey, Newark, and Division of Gastroenterology, Department of Medicine, Jersey City Medical Center, Jersey City,4 New Jersey

Received 16 September 1999/Returned for modification 8 November 1999/Accepted 22 November 1999

Fas-mediated gastric mucosal apoptosis is gaining attention as a cause of tissue damage due to Helicobacter pylori infection. We explored the effects of H. pylori directly, and the effects of the inflammatory environment established subsequent to H. pylori infection, on Fas-mediated apoptosis in a nontransformed gastric mucosal cell line (RGM-1). Exposure to H. pylori-activated peripheral blood mononuclear cells (PBMCs), but not H. pylori itself, induced Fas antigen (Fas Ag) expression, indicating a Fas-regulatory role for inflammatory cytokines in this system. Of various inflammatory cytokines tested, only interleukin 1beta and tumor necrosis factor alpha induced Fas Ag expression, and removal of either of these from the conditioned medium abrogated the response. When exposed to Fas ligand, RGM-1 cells treated with PBMC-conditioned medium underwent massive and rapid cell death, interestingly, with a minimal effect on total cell numbers early on. Cell cycle analysis revealed a substantial increase in S phase cells among cells exposed to Fas ligand, suggesting an increase in their proliferative response. Taken together, these data indicate that the immune environment secondary to H. pylori infection plays a critical role in priming gastric mucosal cells to undergo apoptosis or to proliferate based upon their Fas Ag status.

* Corresponding author. Mailing address: UMDNJ-NJMS, MSB H 528, 185 South Orange Ave., Newark, NJ 07103. Phone: (973) 972-5044. Fax: (973) 972-3644. E-mail: houghtjm{at}umdnj.edu.

Infection and Immunity, March 2000, p. 1189-1195, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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