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Articles in PresS, published online ahead of print February 7, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00766.2001
Submitted on December 28, 2001
Accepted on February 1, 2002
1 Department of Medical Pharmacology, Research Institute Neurosciences Free University, Amsterdam, Netherlands
* To whom correspondence should be addressed. E-mail: a.ledeboer.pharm{at}med.vu.nl.
Bacterial lipopolysaccharide (LPS) induces fever that is mediated by pyrogenic cytokines such as interleukin (IL)-1ß. We hypothesized that the anti-inflammatory cytokine IL-10 modulates the febrile response to LPS by suppressing the production of pyrogenic cytokines. In rats, intravenous (i.v.), but not intracerebroventricular (i.c.v.) infusion of IL-10 was found to attenuate fever induced by peripheral administration of LPS (10 µg/kg, i.v.). IL-10 also suppressed LPS-induced IL-1ß production in peripheral tissues and in the brainstem. In contrast, central administration of IL-10 attenuated the febrile response to central LPS (60 ng/rat, i.c.v.), and decreased IL-1ß production in the hypothalamus and brainstem, but not in peripheral tissues and plasma. Furthermore, i.v. LPS upregulated expression of IL-10 receptor (IL-10R1) mRNA in the liver, whereas i.c.v. LPS enhanced IL-10R1 mRNA in the hypothalamus. We conclude that IL-10 modulates the febrile response by acting in the periphery or in the brain dependent on the primary site of inflammation, and that its mechanism of action most likely involves inhibition of local IL-1ß production.
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