Central mediators involved in the febrile response induced by polyinosinic-polycytidylic acid: Lack of involvement of endothelins and substance P

A. L. Bastos-Pereira, M. C.G. Leite, D. Fraga, A. R. Zampronio

Research output: Contribution to journalArticlepeer-review

15 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)100-107
Number of pages8
JournalJournal of Neuroimmunology
Volume278
DOIs
Publication statusPublished - Jan 15 2015
Externally publishedYes

Bibliographical note

Funding Information:
D. Fraga present address: Faculty of Nursing, Federal University of Mato Grosso do Sul, Coxim, MS, Brazil. This study was supported by the Araucária Foundation of the State of Paraná (grant # 413/09 15188 ) and the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq, grant # 473873/2011-7 ), Brazil. D. Fraga had a post-doctorate scholarship from REUNI , Federal University of Paraná (grant # 23075.085709/2011-60 ).

Publisher Copyright:
© 2014.

ASJC Scopus Subject Areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

PubMed: MeSH publication types

  • Journal Article
  • Research Support, Non-U.S. Gov't

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