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1 Institut National de la Recherche Agronomique-Institut National de la Santé et de la Recherche Médicale Unité 394, Neurobiologie Intégrative, 33077 Bordeaux, France; and 2 Laboratory of Immunophysiology, Department of Animal sciences, University of Illinois, Urbana, Illinois 61801
The present study was designed to determine the role of
endogenous brain interleukin (IL)-1 in the anorexic response to
lipopolysaccharide (LPS). Intraperitoneal administration of LPS
(5-10 µg/mouse) induced a dramatic, but transient, decrease in
food intake, associated with an enhanced expression of proinflammatory
cytokine mRNA (IL-1
, IL-6, and tumor necrosis factor-
)
in the hypothalamus. This dose of LPS also increased plasma levels of
IL-1. Intracerebroventricular pretreatment with IL-1 receptor
antagonist (4 µg/mouse) attenuated LPS-induced depression of food
intake and totally blocked the LPS-induced enhanced expression of
proinflammatory cytokine mRNA measured in the hypothalamus 1 h after
treatment. In contrast, LPS-induced increases in plasma levels of
IL-1 were not altered. These findings indicate that endogenous brain
IL-1 plays a pivotal role in the development of the hypothalamic
cytokine response to a systemic inflammatory stimulus.
hypothalamus; lipopolysaccharide; interleukin-1; receptor antagonist; food intake
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