Neural pathways involved in infection-induced inflammation: recent insights and clinical implications
Clin Auton Res. 2018-03-14; 28(3): 289-299
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1. Clin Auton Res. 2018 Jun;28(3):289-299. doi: 10.1007/s10286-018-0518-y. Epub 2018
Neural pathways involved in infection-induced inflammation: recent insights and
Griton M(1), Konsman JP(2)(3).
(1)Service de Réanimation Anesthésie Neurochirurgicale, Centre Hospitalier
Universitaire (CHU) de Bordeaux, Bordeaux, France.
(2)INCIA, Institut de Neurosciences Cognitive et Intégrative d’Aquitaine, UMR
5287, Bordeaux, France. .
(3)University of Bordeaux, INCIA, UMR 5287, Bordeaux, France.
Although the immune and nervous systems have long been considered independent
biological systems, they turn out to mingle and interact extensively. The present
review summarizes recent insights into the neural pathways activated by and
involved in infection-induced inflammation and discusses potential clinical
applications. The simplest activation concerns a reflex action within C-fibers
leading to neurogenic inflammation. Low concentrations of pro-inflammatory
cytokines or bacterial fragments may also act on these afferent nerve fibers to
signal the central nervous system and bring about early fever, hyperalgesia and
sickness behavior. In the brain, the preoptic area and the paraventricular
hypothalamus are part of a neuronal network mediating sympathetic activation
underlying fever while brainstem circuits play a role in the reduction of food
intake after systemic exposure to bacterial fragments. A vagally-mediated
anti-inflammatory reflex mechanism has been proposed and, in turn, questioned
because the major immune organs driving inflammation, such as the spleen, are not
innervated by vagal efferent fibers. On the contrary, sympathetic nerves do
innervate these organs and modulate immune cell responses, production of
inflammatory mediators and bacterial dissemination. Noradrenaline, which is both
released by these fibers and often administered during sepsis, along with
adrenaline, may exert pro-inflammatory actions through the stimulation of β1
adrenergic receptors, as antagonists of this receptor have been shown to exert
anti-inflammatory effects in experimental sepsis.