Neutralization of macrophage inflammatory protein-2 blocks the febrile response induced by lipopolysaccharide in rats |
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Authors: | Eva Tavares, Maria L. Ojeda, Rosario Maldonado,Francisco J. Mi ano |
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Affiliation: | aResearch Unit, Laboratory for Clinical and Experimental Pharmacology, Valme University Hospital, Seville 41014, Spain bDepartment of Pharmacology, Radiology and Paediatrics, School of Medicine, University of Seville, Seville 41009, Spain |
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Abstract: | 1. This study was aimed to test the hypothesis that macrophage inflammatory protein-2 (MIP-2), a powerful chemotactic cytokine for neutrophils, plays a role in bacterial endotoxin fever. 2. The effect of specific anti-rat MIP-2 antibodies on lipopolysaccharide (LPS)-induced fever was tested. Intraperitoneal injection of LPS resulted in a biphasic fever and a significant increase in serum MIP-2 and prostaglandin (PG) E2 levels which correlated with the start of fever. Intraperitoneal anti-MIP-2 (500 μg/kg) did not affect the body core temperature of unrestrained rats, but markedly attenuated LPS-induced fever. 3. Treatment with the cyclooxygenase inhibitor ibuprofen (10 mg/kg) resulted in a significant attenuation of LPS-induced fever and a significant decrease of MIP-2 and PGE2 production. 4. These results indicate that LPS fever in rats is, at least, in part dependent on mechanisms involving neutrophils chemotaxis, and that MIP-2 may be an important mediator in the genesis of fever via prostaglandin-dependent pathways. |
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Keywords: | Fever Ibuprofen MIP-2 PGE2 Rats |
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