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Regulation by interleukin-10 and interleukin-4 of cyclooxygenase-2
expression in human neutrophils
H Niiro, T Otsuka, K Izuhara, K Yamaoka, K Ohshima, T Tanabe, S Hara, Y Nemoto, Y Tanaka, H Nakashima and Y Niho
First Department of Internal Medicine, Faculty of Medicine, Kyushu
University, Fukuoka, Japan.
Neutrophils are important effector cells of acute inflammation because of
their potential capacity to synthesize various proinflammatory mediators,
and inhibition of their production is expected to result in
anti-inflammatory effects. In this study, we investigate the effects of the
anti-inflammatory cytokines, interleukin-10 (IL-10) and IL-4, on prostanoid
synthesis in human neutrophils. Neutrophils isolated from healthy donors
constitutively produced a small amount of prostaglandin E2 (PGE2) without
any stimulations, whereas they produced a large amount of PGE2 after
lipopolysaccharide (LPS) stimulation. IL-10 and IL- 4 selectively inhibited
their LPS-induced PGE2 production. Inhibition by both cytokines occurred at
an early stage of LPS stimulation. Anti- IL-10 treatment of LPS-stimulated
neutrophils resulted in enhanced PGE2 production. LPS-induced PGE2 and
thromboxane B2 (TXB2) production in aspirin-treated neutrophils was
significantly inhibited by IL-10, IL-4, and NS-398. Moreover, IL-10 and
IL-4 inhibited LPS-induced cyclooxygenase (COX) activity in neutrophils.
Western blot and immunocytochemical analysis showed that COX-2 protein was
clearly induced in LPS-stimulated neutrophils and that its induction was
inhibited by both IL-10 and IL-4. Moreover, both of these cytokines
inhibited COX-2 mRNA expression in LPS-stimulated neutrophils. These
results raise the possibility that these two cytokines may both offer
potent clinical utility as anti-inflammatory agents in the future.
Volume 89,
Issue 5,
pp. 1621-1628,
03/01/1997
Copyright © 1997 by The American Society of Hematology
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