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in Mouse Macrophages1
*
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205; and
Department of Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109
Turnover of the extracellular matrix (ECM), activation of
macrophages, and accumulation of chemokines/cytokines are all hallmarks
of chronic inflammation. Extracellular matrix components, such as
hyaluronan (HA), have recently been shown to influence macrophage
effector functions, such as the release of inflammatory chemokines and
cytokines. Although low m.w. fragments of the glycosaminoglycan HA
induce macrophages to secrete numerous inflammatory mediators, the
mechanisms regulating ECM-induced macrophage activation are poorly
understood. We have examined the effects of IL-10 and IFN-
on
HA-induced chemokine gene expression in primary mouse macrophages. We
found that IL-10 and IFN- independently inhibit HA-induced
expression of macrophage inflammatory protein-1
(MIP-1),
MIP-1ß, and KC at both the mRNA and protein levels. Whereas IL-10
inhibited most of the HA-induced chemokines tested, IFN- selectively
inhibited only MIP-1, MIP-1ß, and KC. This inhibition did not
require prestimulation and occurred even when the cytokines were added
up to 3 h after stimulation with HA. For MIP-1, the inhibition
by IFN- occurred at the level of transcription, whereas IL-10
predominantly decreased the stability of MIP-1 mRNA. IFN- and
IL-10 equally inhibited macrophage expression of MIP-1ß mRNA at the
level of transcription, but MIP-1ß mRNA stability was decreased to a
greater extent by IL-10. These data identify a previously unrecognized
role for IL-10 and IFN- as regulators of ECM-induced macrophage
expression of inflammatory chemokines.
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