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*
Department of Medicine, Laval University Heart and Lung Institute, Laval Hospital, Ste-Foy, Quebec, Canada; and
Department of Medicine, Pulmonary Research Group, University of Alberta, Edmonton, Alberta, Canada
Histamine, a well-known inflammatory mediator, has been implicated
in various immunoregulatory effects that are poorly understood. Thus,
we tested the hypothesis that histamine inhibits the release of a
proinflammatory cytokine, namely TNF, by stimulating the release of an
anti-inflammatory cytokine, IL-10. Alveolar macrophages (AMs) from
humans, Sprague Dawley rats, and the AM cell line, NR8383, were treated
with different concentrations of histamine
(10-5-10-7 M) for 2 h prior to their
stimulation with suboptimal concentration of LPS (1 ng/ml) for 4
h. Histamine inhibited TNF release in a dose-dependent manner. This
inhibition was mimicked by H2 and H3 receptor
agonists, but not by H1 receptor agonist. Furthermore, we
demonstrated the expression of H3 receptor mRNA in human
AMs. Interestingly, treatment of AMs with anti-IL-10,
anti-PGE2, or a NO synthase inhibitor
(N
-nitro-L-arginine methyl
ester) before the addition of histamine abrogated the inhibitory effect
of the latter on TNF release. Histamine treatment (10-5 M)
increased the release of IL-10 from unstimulated (2.2-fold) and
LPS-stimulated (1.7-fold) AMs. Unstimulated AMs, NR8383, express few
copies of IL-10 mRNA, as tested by quantitative PCR, but expression of
IL-10 was increased by 1.5-fold with histamine treatment. Moreover, the
stimulation of IL-10 release by histamine was abrogated by pretreatment
with anti-PGE2 or the NO synthase inhibitor,
N-nitro-L-arginine methyl ester. Thus,
histamine increases the synthesis and release of IL-10 from AMs through
PGE2 and NO production. These results suggest that
histamine may play an important role in the modulation of the cytokine
network.
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