Neural reflex regulation of systemic inflammation: potential new targets for sepsis therapy
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Fecha
2014
Profesor/a Guía
Facultad/escuela
Idioma
en
Título de la revista
ISSN de la revista
Título del volumen
Editor
Frontiers Media S.A.
Nombre de Curso
Licencia CC
Atribution 4.0 International (CC BY 4.0)
Licencia CC
Resumen
Sepsis progresses to multiple organ dysfunction due to the uncontrolled release of
inflammatory mediators, and a growing body of evidence shows that neural signals play a
significant role in modulating the immune response. Thus, similar toall other physiological
systems, the immune system is both connected to and regulated by the central nervous
system. The efferent arc consists of the activation of the hypothalamic–pituitary–adrenal
axis, sympathetic activation, the cholinergic anti-inflammatory reflex, and the local release
of physiological neuromodulators. Immunosensory activity is centered on the production
of pro-inflammatory cytokines, signals that are conveyed to the brain through different
pathways. The activation of peripheral sensory nerves, i.e., vagal paraganglia by the
vagus nerve, and carotid body (CB) chemoreceptors by the carotid/sinus nerve are
broadly discussed here. Despite cytokine receptor expression in vagal afferent fibers,
pro-inflammatory cytokines have no significant effect on vagus nerve activity. Thus, the
CB may be the source of immunosensory inputs and incoming neural signals and, in
fact, sense inflammatory mediators, playing a protective role during sepsis. Considering
that CB stimulation increases sympathetic activity and adrenal glucocorticoids release, the
electrical stimulation of arterial chemoreceptors may be suitable therapeutic approach for
regulating systemic inflammation
Notas
Indexación: Scopus.
Palabras clave
Systemic Inflammation, Sepsis, Reflex Control of Inflammation, Carotid Body, Vagus Nerve
Citación
Frontiers in Physiology. Volume 5, Issue DEC. 2014. Article number 489
DOI
10.3389/fphys.2014.00489