Febrile response induced by cecal ligation and puncture (CLP) in rats: involvement of prostaglandin E2 and cytokines
| Autor: | Maria José, Figueiredo, Denis Melo, Soares, Denis de Melo, Soares, Juliano Manvailer, Martins, Renes de Resende, Machado, Carlos Arterio, Sorgi, Lucia Helena, Faccioli, Miriam Cristina Contin de, Melo, Miriam Cristina Contin, de Melo, David do Carmo, Malvar, Glória E P, Souza |
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| Rok vydání: | 2012 |
| Předmět: |
Male
Microbiology (medical) medicine.medical_specialty Fever Immunology Prostaglandin Punctures Peritonitis Dinoprostone chemistry.chemical_compound Cerebrospinal fluid Internal medicine medicine MODELOS ANIMAIS DE DOENÇAS Animals Humans Immunology and Allergy Antipyretic Rats Wistar Prostaglandin E2 Cecum Ligation Bacteria business.industry Peritoneal fluid Interleukin Bacterial Infections General Medicine Survival Analysis Bacterial Load Rats Disease Models Animal Blood Endocrinology chemistry Hypothalamus Cytokines Tumor necrosis factor alpha Peritoneum business medicine.drug |
| Zdroj: | Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual) Universidade de São Paulo (USP) instacron:USP |
| Popis: | The purpose of the present study was to better understand the events involved in the febrile response induced by cecal ligation and puncture (CLP), a complex infectious process. To this end, we conducted in vivo experiments in rats examining (1) fever development, (2) bacterial number in the infection focus and in blood, (3) peripheral and hypothalamic synthesis of cytokines, (4) hypothalamic and cerebrospinal fluid (CSF) synthesis of prostaglandin E(2) (PGE(2)), (5) the effect of anti-IL-6 antibody on fever, and (6) the effect of celecoxib on fever and hypothalamic synthesis of PGE(2) after CLP induction. We found that CLP promotes fever and animal death depending on the number of punctures. The peak of CLP-induced fever overlapped with the maximal increase in the number of bacteria in the infectious focus and blood, which occurred at 6 and 12 h. The peak of the febrile response also coincided with increased amounts of interleukin (IL)-1β, IL-6 and IL-10 in the peritoneal exudate and serum; IL-6 in the hypothalamus and PGE(2) in the CSF and predominantly in the hypothalamus. Moreover, intracerebroventricularly injected anti-IL-6 antibody reduced the febrile response while celecoxib reduced the fever and PGE(2) amount in the hypothalamus induced by CLP. Tumor necrosis factor (TNF)-α peaked at 3 h at all sites studied. Conversely, IL-10 concentration decreased in the hypothalamus. These findings show that the peak of CLP-induced fever is accompanied by an increase of bacteria in peritoneal fluid (local infection) and blood; local synthesis of pyrogenic (IL-1β, IL-6) and antipyretic (IL-10) cytokines and central production of IL-6 and PGE(2), suggesting that these last are the central mediators of this response. |
| Databáze: | OpenAIRE |
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