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,
,¶,*
,¶
* Department of Medicine, Division of Gastroenterology, Departments of
Surgery and
Pathology, and
Greenebaum Cancer Center, University of Maryland School of Medicine, and
¶ Veterans Affairs Maryland Health Care System, Baltimore, MD 21201;
|| Laboratoire de Chimie et Biochimie Pharmacologiques, Unité Mixte de Recherche 8601, Centre National de la Recherche Scientifique, Université René Descartes, Paris, France;
# Department of Pathology and Laboratory Medicine,
** Mental Retardation Research Center, Departments of
Psychiatry and
* Pediatrics, University of California School of Medicine, Los Angeles, CA 90024; and
* Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD 21231
Helicobacter pylori infection induces innate immune
responses in macrophages, contributing to mucosal inflammation and
damage. Macrophage apoptosis is important in the pathogenesis of
mucosal infections but has not been studied with H.
pylori. NO derived from inducible NO synthase (iNOS) can
activate macrophage apoptosis. Arginase competes with iNOS by
converting L-arginine to L-ornithine. Since we
reported that H. pylori induces iNOS in macrophages, we
now determined whether this bacterium induces arginase and the effect
of this activation on apoptosis. NF-
B-dependent induction of
arginase II, but not arginase I, was observed in RAW 264.7 macrophages
cocultured with H. pylori. The time course of apoptosis
matched those of both arginase and iNOS activities. Surprisingly,
apoptosis was blocked by the arginase inhibitors
N
-hydroxy-L-arginine
or
N-hydroxy-nor-L-arginine,
but not by the iNOS inhibitor
N-iminoethyl-L-lysine. These findings
were confirmed in peritoneal macrophages from iNOS-deficient mice and
were not dependent on bacterial-macrophage contact. Ornithine
decarboxylase (ODC), which metabolizes L-ornithine to
polyamines, was also induced in H. pylori-stimulated
macrophages. Apoptosis was abolished by inhibition of ODC and was
restored by the polyamines spermidine and spermine. We also demonstrate
that arginase II expression is up-regulated in both murine and human
H. pylori gastritis tissues, indicating the likely in
vivo relevance of our findings. Therefore, we describe arginase- and
ODC-dependent macrophage apoptosis, which implicates polyamines in the
pathophysiology of H. pylori
infection.
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