title: Central mediators involved in the febrile response induced by polyinosinic-polycytidylic acid: lack of involvement of endothelins and substance P.
abstract: The present study evaluated the involvement of interleukin(IL)-1β, tumor necrosis factor-α (TNF-α), IL-6, interferon(IFN)-γ, prostaglandins of the E2 series, endothelins, substance P and opioids within the central nervous system in polyinosinic:polycytidylic acid (Poly I:C)-induced fever in rats. Poly I:C injection induced a febrile response which was reduced by intracerebroventricular administration of the antibodies against TNF-α, IL-6, or IFN-γ, or by IL-1 or μ receptor antagonists. Intraperitoneal injection of indomethacin or oral administration of celecoxib also reduced Poly I:C-induced fever. Poly I:C increased prostaglandin E2 levels in the cerebrospinal fluid of the animals which was also reduced by indomethacin. The intracerebroventricular injection of ETB or NK1 receptor antagonists did not alter Poly I:C-induced fever. These data suggest the involvement of IL-1β, TNF-α, IL-6, IFN-γ, prostaglandin E2, and opioids but not endothelins and substance P on Poly I:C-induced fever.
authors.affiliation: Department of Pharmacology, Federal University of Paraná, P.O. Box 19031, 81540-970 Curitiba, PR, Brazil.
authors.forename: A L
authors.initials: AL
authors.lastname: Bastos-Pereira
authors.affiliation: Department of Pharmacology, Federal University of Paraná, P.O. Box 19031, 81540-970 Curitiba, PR, Brazil.
authors.forename: M C G
authors.initials: MC
authors.lastname: Leite
authors.affiliation: Department of Pharmacology, Federal University of Paraná, P.O. Box 19031, 81540-970 Curitiba, PR, Brazil.
authors.forename: D
authors.initials: D
authors.lastname: Fraga
authors.affiliation: Department of Pharmacology, Federal University of Paraná, P.O. Box 19031, 81540-970 Curitiba, PR, Brazil. Electronic address: aleksander@ufpr.br.
authors.forename: A R
authors.initials: AR
authors.lastname: Zampronio
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal; D000906:Antibodies / Q000627:therapeutic use; D001831:Body Temperature / Q000187:drug effects; D000068579:Celecoxib; D002490:Central Nervous System / Q000187:drug effects / Q000378:metabolism*; D016207:Cytokines / Q000276:immunology / Q000378:metabolism*; D015232:Dinoprostone / Q000378:metabolism*; D065131:Endothelin B Receptor Antagonists / Q000627:therapeutic use; D005334:Fever / Q000139:chemically induced*; D007213:Indomethacin / Q000627:therapeutic use; D007369:Interferon Inducers / Q000633:toxicity*; D008297:Male; D009842:Oligopeptides / Q000627:therapeutic use; D010455:Peptides; D010880:Piperidines / Q000627:therapeutic use; D011070:Poly I-C / Q000633:toxicity*; D011720:Pyrazoles / Q000627:therapeutic use; D051381:Rats; D017208:Rats, Wistar; D013449:Sulfonamides / Q000627:therapeutic use; D014326:Tropanes / Q000627:therapeutic use
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000906:Antibodies; D016207:Cytokines; D065131:Endothelin B Receptor Antagonists; D007369:Interferon Inducers; D009842:Oligopeptides; D010455:Peptides; D010880:Piperidines; D011720:Pyrazoles; C526005:SR140333B; D013449:Sulfonamides; D014326:Tropanes; C086539:BQ 788; C009862:connective tissue-activating peptide; D000068579:Celecoxib; D015232:Dinoprostone; D011070:Poly I-C; D007213:Indomethacin
keywords: Cytokine; Endothelin; Opioids; Poly I:C; Prostaglandin; Substance P