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Fever: causes and consequences
1University of Chicago, IL 60637.
Abstract:
The present review distinguishes pathogenic, neurogenic, and psychogenic fever, but focuses largely on pathogenic fever, the hallmark of infectious disease. The data presented show that a complex cascade of events underlies pathogenic fever, which in broad outline - and with frank disregard of contradictory data - can be described as follows. An invading microorganism releases endotoxin that stimulates macrophages to synthesize a variety of pyrogenic compounds called cytokines. Carried in blood, these cytokines reach the perivascular spaces of the organum vasculosum laminae terminalis (OVLT) and other regions near the brain where they promote the synthesis and release of prostaglandin (PGE2). This prostaglandin then penetrates the blood-brain barrier to evoke the autonomic and behavioral responses characteristic of fever. But then once expressed, fever does not continue unchecked; endogenous antipyretics likely act on the septum to limit the rise in body temperature. The present review also examines fever-resistance in neonates, the blunting of fever in the aged, and the behaviorally induced rise in body temperature following infection in ectotherms. And finally it takes up the question of whether fever enhances immune responsiveness, and through such enhancement contributes to host survival.
Insights
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.
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.