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2018 ; 24
(4
): 381-399
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Neural Mechanisms of Inflammation-Induced Fever
#MMPMID29557255
Blomqvist A
; Engblom D
Neuroscientist
2018[Aug]; 24
(4
): 381-399
PMID29557255
show ga
Fever is a common symptom of infectious and inflammatory disease. It is
well-established that prostaglandin E(2) is the final mediator of fever, which by
binding to its EP(3) receptor subtype in the preoptic hypothalamus initiates
thermogenesis. Here, we review the different hypotheses on how the presence of
peripherally released pyrogenic substances can be signaled to the brain to elicit
fever. We conclude that there is unequivocal evidence for a humoral signaling
pathway by which proinflammatory cytokines, through their binding to receptors on
brain endothelial cells, evoke fever by eliciting prostaglandin E(2) synthesis in
these cells. The evidence for a role for other signaling routes for fever, such
as signaling via circumventricular organs and peripheral nerves, as well as
transfer into the brain of peripherally synthesized prostaglandin E(2) are yet
far from conclusive. We also review the efferent limb of the pyrogenic pathways.
We conclude that it is well established that prostaglandin E(2) binding in the
preoptic hypothalamus produces fever by disinhibition of presympathetic neurons
in the brain stem, but there is yet little understanding of the mechanisms by
which factors such as nutritional status and ambient temperature shape the
response to the peripheral immune challenge.
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