Fever and hypothermia in systemic inflammation: recent discoveries and revisions.
Level 5 - mechanism / opinion, no new human data
Narrative review of animal models and mechanistic pathways without primary human data.
PubMed 15970487 · doi:10.2741/1690
What was done
This narrative review synthesizes research on the molecular mediators, neural pathways, and regulatory concepts governing fever and hypothermia during systemic inflammation, focusing on rodent models, genetic knockouts, and lipopolysaccharide-induced signaling.
What was found
The abstract reports no numerical or quantitative data. It outlines several mechanistic models: peripheral inflammatory signals cross the blood-brain barrier via active transduction into prostaglandin E2 (PGE2) through inducible COX-2 and mPGES-1; PGE2 acts via preoptic EP3 receptors projecting to the raphe pallidus to drive thermoeffectors; and thermoregulation during inflammation reflects a dynamic balance point rather than a fixed set point.
Why it matters
It clarifies the central pathways transducing peripheral inflammation into thermal responses, pointing to specific downstream targets such as mPGES-1 for antipyretic drug development beyond non-selective COX inhibitors.
Limits
The abstract provides no quantitative data, search parameters, or study counts. Findings are largely derived from rodent and in vitro models, limiting direct translation to human systemic inflammatory response syndrome and sepsis.
Cited by
- supports Immune cells secrete cytokines into the bloodstream that act as distributed chemical signals capable of inducing systemic responses like fever.