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Cytokines and fever

C M Blatteis1, E Sehic

  • 1Department of Physiology and Biophysics, University of Tennessee, Memphis 38163, USA. blatteis@physio1.utmem.edu

Annals of the New York Academy of Sciences
|June 18, 1998
PubMed
Summary

Fever is triggered by pathogens and involves cytokines signaling the brain. This study proposes a novel pathway involving norepinephrine and prostaglandin E2 (PGE2) in the hypothalamus to initiate fever responses.

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Area of Science:

  • Neuroscience
  • Immunology
  • Physiology

Background:

  • Fever is an immune response to pathogens, typically mediated by cytokines acting on the brain.
  • The precise signaling pathway from peripheral infection to central fever induction remains unclear.
  • Complex cytokine interactions and varied responses to different pyrogens complicate understanding.

Purpose of the Study:

  • To elucidate the detailed mechanism of fever induction by lipopolysaccharide (LPS).
  • To investigate the role of norepinephrine (NE) and prostaglandin E2 (PGE2) in LPS-induced fever.
  • To propose a novel signaling cascade for fever initiation.

Main Methods:

  • Utilized guinea pig models with interventions like subdiaphragmatic vagotomy, decomplementation, and Kupffer cell blockade.
  • Administered intravenous LPS to induce fever.
  • Measured norepinephrine (NE) and PGE2 levels in the preoptic-anterior hypothalamus (POA).

Main Results:

  • Subdiaphragmatic vagotomy, decomplementation, and Kupffer cell blockade suppressed LPS-induced fever.
  • Intravenous LPS rapidly stimulated NE and PGE2 release in the POA.
  • Cytokine levels (IL-6, IL-1, TNF alpha) showed delayed increases and smaller magnitude compared to fever onset.

Conclusions:

  • LPS-induced fever involves a pathway initiated peripherally, potentially involving complement and Kupffer cells.
  • Vagal afferents transmit signals to the brainstem, leading to NE release in the POA.
  • Norepinephrine (NE) stimulates PGE2 production in the POA, ultimately triggering the febrile response.

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