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Infection and Immunity, November 2000, p. 6265-6272, Vol. 68, No. 11
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Modulation of Innate Cytokine Responses by Products of Helicobacter pylori

Frank Meyer,dagger Keith T. Wilson, and Stephen P. James*

Division of Gastroenterology, Department of Medicine, University of Maryland, and the Baltimore Veterans Administration Medical System, Baltimore, Maryland

Received 12 May 2000/Returned for modification 15 June 2000/Accepted 27 August 2000

The gastric inflammatory and immune response in Helicobacter pylori infection may be due to the effect of different H. pylori products on innate immune mechanisms. The aim of this study was to determine whether bacterial components could modulate cytokine production in vitro and thus contribute to Th1 polarization of the gastric immune response observed in vivo. The effect of H. pylori recombinant urease, bacterial lysate, intact bacteria, and bacterial DNA on proliferation and cytokine production by peripheral blood mononuclear cells (PBMCs) from H. pylori-negative donors was examined as a model for innate cytokine responses. Each of the different H. pylori preparations induced gamma interferon (IFN-gamma ) and interleukin-12p40 (IL-12p40), but not IL-2 or IL-5, production, and all but H. pylori DNA stimulated release of IL-10. Addition of anti-IL-12 antibody to cultures partially inhibited IFN-gamma production. In addition, each bacterial product inhibited mitogen-stimulated IL-2 production by PBMCs and Jurkat T cells. The inhibitory effect of bacterial products on IL-2 production correlated with inhibition of mitogen-stimulated lymphocyte proliferation, although urease inhibited IL-2 production without inhibiting proliferation, suggesting that inhibition of IL-2 production alone is not sufficient to inhibit lymphocyte proliferation. The results of these studies demonstrate that Th1 polarization of the gastric immune response may be due in part to the direct effects of multiple different H. pylori components that enhance IFN-gamma and IL-12 production while inhibiting both IL-2 production and cell proliferation that may be necessary for Th2 responses.

* Corresponding author. Mailing address: Division of Gastroenterology, Department of Medicine, University of Maryland, Room N3W62, 22 S. Greene St., Baltimore, MD 21201. Phone: (410) 328-8728. Fax: (410) 328-8315. E-mail: sjames{at}medicine.umaryland.edu.

dagger Present address: Department of Surgery, University Hospital, Otto von Guericke University, D-39120 Magdeburg, Germany.

Infection and Immunity, November 2000, p. 6265-6272, Vol. 68, No. 11
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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