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-Adrenergic agonists exert their
"anti-inflammatory" effects in monocytic cells through the
I
B/NF-B pathway
Division of Medical Intensive Care, Department of Internal Medicine, University Hospital of Geneva, 1211 Geneva 14, Switzerland
In addition
to their well-studied bronchodilatory and cardiotonic effects,
-adrenergic agonists carry anti-inflammatory properties by
inhibiting cytokine production by human mononuclear cells. In a model
of human promonocytic THP-1 cells stimulated with lipopolysaccharide
(LPS), we showed that -agonists inhibited tumor necrosis factor-
and interleukin-8 production predominantly via the
2-adrenergic receptor through the generation of cAMP and
activation of protein kinase A. This effect was reproduced by other
cAMP-elevating agents such as prostaglandins and cAMP analogs.
Activation and nuclear translocation of the transcription factor
nuclear factor-
B induced by LPS were inhibited with treatment with
-agonists, an effect that was prominent at late time points (>1 h).
Although the initial IB- degradation induced by LPS was minimally
affected by -agonists, the latter induced a marked rebound of the
cytosolic IB- levels at later time points (>1 h), accompanied by
an increased IB- cytoplasmic half-life. This potentially accounts
for the observed nuclear factor-B sequestration in the cytoplasmic
compartment. We postulate that the anti-inflammatory effects of
-agonists reside in their capacity to increase cytoplasmic concentrations of IB-, possibly by decreasing its degradation.
lipopolysaccharide; nuclear factor-B; IB; adenosine
3',5'-cyclic monophosphate
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