Learn More
The innate immune system serves as the first line of host defense against the deleterious effects of invading infectious pathogens. Fever is the hallmark among the defense mechanisms evoked by the entry into the body of such pathogens. The conventional view of the steps that lead to fever production is that they begin with the biosynthesis of pyrogenic(More)
Norepinephrine (NE) microdialyzed in the preoptic area (POA) raises core temperature (T(c)) via 1) alpha(1)-adrenoceptors (AR), quickly and independently of POA PGE(2), and 2) alpha(2)-AR, after a delay and PGE(2) dependently. Since systemic lipopolysaccharide (LPS) activates the central noradrenergic system, we investigated whether preoptic NE mediates LPS(More)
Because the onset of fever induced by intravenously (i.v.) injected bacterial endotoxic lipopolysaccharides (LPS) precedes the appearance in the bloodstream of pyrogenic cytokines, the presumptive peripheral triggers of the febrile response, we have postulated previously that, in their stead, PGE2 could be the peripheral fever trigger because it appears in(More)
We have shown previously that norepinephrine (NE) microdialyzed into the preoptic area (POA) of conscious guinea pigs stimulates local PGE(2) release. To identify the cyclooxygenase (COX) isozyme that catalyzes the production of this PGE(2) and the adrenoceptor (AR) subtype that mediates this effect, we microdialyzed for 6 h NE, cirazoline (alpha(1)-AR(More)
The febrile responses of splenectomized (Splex) or sham-operated (Sham) guinea pigs challenged intravenously or intraperitoneally with lipopolysaccharide (LPS) 7 and 30 days after surgery were evaluated. FITC-LPS uptake by Kupffer cells (KC) was additionally assessed 15, 30, and 60 min after injection. LPS at 0.05 microg/kg iv did not evoke fever in Sham(More)
We reported previously that the onset of LPS-induced fever, irrespective of its route of administration, is temporally correlated with the appearance of LPS in the liver and that splenectomy significantly increases both the febrile response to LPS and the uptake of LPS by Kupffer cells (KC). To further evaluate the role of the spleen in LPS fever(More)
The complement (C) cascade is activated in almost immediate reaction to the appearance in the body of pathogenic microorganims and their products, e.g., bacterial endotoxic lipopolysaccharide (LPS), resulting in the generation of a series of potent bioactive fragments that have critical roles in the innate immune response of the afflicted host, including,(More)
The intravenous injection of LPS rapidly evokes fever. We have hypothesized that its onset is mediated by prostaglandin (PG)E(2) quickly released by Kupffer cells (Kc). LPS, however, does not stimulate PGE(2) production by Kc as rapidly as it induces fever; but complement (C) activated by LPS could be the exciting agent. To test this hypothesis, we injected(More)
Lipopolysaccharide (LPS) administration induces hypothalamic nitric oxide (NO); NO is antipyretic in the preoptic area (POA), but its mechanism of action is uncertain. LPS also stimulates the release of preoptic norepinephrine (NE), which mediates fever onset. Because NE upregulates NO synthases and NO induces cyclooxygenase (COX)-2-dependent PGE(2), we(More)
Li, Zhonghua, Vit Perlik, Carlos Feleder, Ying Tang, and Clark M. Blatteis. Kupffer cell-generated PGE2 triggers the febrile response of guinea pigs to intravenously injected LPS. Am J Physiol Regul Integr Comp Physiol 290: R1262–R1270, 2006. First published January 12, 2006; doi:10.1152/ajpregu.00724.2005.—Because the onset of fever induced by(More)