Central mediators of the zymosan-induced febrile response

Amanda Leite Bastos-Pereira, Daniel Fraga, Arturo Alejandro Dreifuss, Aleksander Roberto Zampronio

Résultat de recherche: Articleexamen par les pairs

9 Citations (Scopus)

Résumé

Zymosan is a fungal cell wall protein-carbohydrate complex that is known to activate inflammatory pathways through the Toll-like receptors and is commonly used to induce fever. Nevertheless, the central mediators that are involved in the zymosan-induced febrile response are only partially known. The present study evaluated the participation of prostaglandins, substance P, endothelin-1 (ET-1), and endogenous opioids (eOPs) in the zymosan-induced febrile response by using inhibitors and antagonists in male Wistar rats. Both nonselective (indomethacin) and selective (celecoxib) cyclooxygenase inhibitors reduced the febrile response induced by an intraperitoneal (i.p.) injection of zymosan. Indomethacin also blocked the increase in the prostaglandin E2 levels in the cerebrospinal fluid. An intracerebroventricular injection of the neurokinin-1, ETB, and μ-opioid receptor antagonists also reduced the febrile response induced by the i.p. injected zymosan. Moreover, the μ-opioid receptor antagonist CTAP also reduced the febrile response induced by intra-articular injection of zymosan. These results demonstrate that prostaglandins, substance P, ET-1, and eOPs are central mediators of the zymosan-induced febrile response.

Langue d'origineEnglish
Pages (de-à)555-562
Nombre de pages8
JournalJournal of Basic and Clinical Physiology and Pharmacology
Volume28
Numéro de publication6
DOI
Statut de publicationPublished - nov. 27 2017
Publié à l'externeOui

Note bibliographique

Funding Information:
Acknowledgments: This study was supported by the Conselho Nacional de Desenvolvimento Científico e Tec-nológico (CNPq), Brazil (Grant No. 473873/2011-7). D. Fraga had a postdoctoral scholarship from REUNI, UFPR. Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission. Research funding: None declared. Employment or leadership: None declared. Honorarium: None declared. Competing interests: The funding organization(s) played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

Publisher Copyright:
© 2017 Walter de Gruyter GmbH, Berlin/Boston.

ASJC Scopus Subject Areas

  • Physiology
  • Pharmacology
  • Drug Discovery

PubMed: MeSH publication types

  • Journal Article

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