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dc.contributor.authorFernandez R.
dc.contributor.authorNardocci G.
dc.contributor.authorNavarro C.
dc.contributor.authorReyes E.P.
dc.contributor.authorAcuña-Castillo C.
dc.contributor.authorCortes P.P.
dc.date.accessioned2020-09-02T22:17:26Z
dc.date.available2020-09-02T22:17:26Z
dc.date.issued2014
dc.identifier10.3389/fphys.2014.00489
dc.identifier.citation5, DEC, -
dc.identifier.issn1664042X
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4436
dc.descriptionSepsis 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. © 2014 Fernandez, Nardocci, Navarro, Reyes, Acuña-Castillo and Cortes.
dc.language.isoen
dc.publisherFrontiers Media S.A.
dc.subjectCarotid body
dc.subjectReflex control of inflammation
dc.subjectSepsis
dc.subjectSystemic inflammation
dc.subjectVagus nerve
dc.subjectglucocorticoid
dc.subjecthypoxia inducible factor
dc.subjecttumor necrosis factor alpha
dc.subjectadrenergic system
dc.subjectcarotid body
dc.subjectcarotid sinus
dc.subjectcorticosteroid release
dc.subjectcytokine production
dc.subjecthuman
dc.subjecthypothalamus hypophysis adrenal system
dc.subjectimmune response
dc.subjectimmune system
dc.subjectimmunomodulation
dc.subjectimmunoreactivity
dc.subjectimmunoregulation
dc.subjectinflammation
dc.subjectnonhuman
dc.subjectparaganglion
dc.subjectprotein expression
dc.subjectreflex
dc.subjectregulatory T lymphocyte
dc.subjectReview
dc.subjectsepsis
dc.subjectsignal transduction
dc.subjectvagus nerve
dc.titleNeural reflex regulation of systemic inflammation: Potential new targets for sepsis therapy
dc.typeReview


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