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in Human Peripheral Blood Mononuclear Cells
Departments of
*
Surgery,
Pharmacology, and
Pathology, Okayama University Medical School, Okayama, Japan
Histamine (10-7 to 10-4 M)
concentration-dependently stimulated the production of IL-18 and
IFN-
and inhibited the production of IL-2 and IL-10 in human PBMCs.
Histamine in the same concentration range did not induce the production
of IL-12 at all. The stimulatory or inhibitory effects of histamine on
cytokine production were all antagonized by H2 receptor
antagonists ranitidine and famotidine in a concentration-dependent
manner, but not by H1 and H3 receptor
antagonists. Selective H2 receptor agonists,
4-methylhistamine and dimaprit, mimicked the effects of histamine on
five kinds of cytokine production. The EC50 values of
histamine, 4-methylhistamine, and dimaprit for the production of IL-18
were 1.5, 1.0, and 3.8 µM, respectively. These findings indicated
that histamine caused cytokine responses through the stimulation of
H2 receptors. All effects of histamine on cytokine
responses were also abolished by the presence of either anti-IL-18
Ab or IL-1ß-converting enzyme/caspase-1 inhibitor, indicating that
the histamine action is dependent on mature IL-18 secretion and that
IL-18 production is located upstream of the cytokine cascade activated
by histamine. The addition of recombinant human IL-18 to the culture
concentration-dependently stimulated IL-12 and IFN- production and
inhibited the IL-2 and IL-10 production. IFN- production induced by
IL-18 was inhibited by anti-IL-12 Ab, showing the marked contrast
of the effect of histamine. Thus histamine is a very important
modulator of Th1 cytokine production in PBMCs and is quite unique in
triggering IL-18-initiating cytokine cascade without inducing IL-12
production.
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