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Fever: causes and consequences

H Moltz1

  • 1University of Chicago, IL 60637.

Neuroscience and Biobehavioral Reviews
|January 1, 1993
PubMed
Summary

Pathogenic fever, a hallmark of infection, involves a cascade initiated by endotoxins stimulating cytokine release. These signal the brain to produce prostaglandin E2 (PGE2), causing fever, which is then regulated by endogenous antipyretics.

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Area of Science:

  • Immunology
  • Neuroscience
  • Physiology

Background:

  • Fever is a complex physiological response often associated with infectious diseases.
  • Understanding the mechanisms of fever is crucial for comprehending host defense strategies.
  • Existing knowledge differentiates types of fever but requires detailed mechanistic insights.

Purpose of the Study:

  • To elucidate the complex cascade underlying pathogenic fever.
  • To explore the roles of cytokines and prostaglandin E2 (PGE2) in fever development.
  • To examine fever regulation, resistance in specific populations, and its impact on immune response.

Main Methods:

  • Review of existing scientific literature on fever pathogenesis.
  • Analysis of the molecular signaling pathways involved in fever induction.
  • Examination of physiological and behavioral responses associated with fever.

Main Results:

  • Pathogenic fever is triggered by microbial endotoxins, leading to macrophage synthesis of pyrogenic cytokines.
  • Cytokines stimulate prostaglandin E2 (PGE2) production in brain regions like the OVLT, crossing the blood-brain barrier.
  • Endogenous antipyretics regulate fever by acting on the septum to limit temperature rise.

Conclusions:

  • Pathogenic fever involves a well-defined signaling cascade from peripheral infection to central thermoregulatory centers.
  • Fever regulation is a dynamic process involving both pyrogenic and antipyretic mechanisms.
  • Further research is needed to fully understand fever's contribution to host survival and immune enhancement.

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