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Infection and Immunity, November 2000, p. 6265-6272, Vol. 68, No. 11
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-
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

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