Neural reflex regulation of systemic inflammation: potential new targets for sepsis therapy.
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 co...
Main Authors: | , , , , , |
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Format: | Article |
Language: | English |
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Frontiers Media S.A.
2014-12-01
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Series: | Frontiers in Physiology |
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Online Access: | http://journal.frontiersin.org/Journal/10.3389/fphys.2014.00489/full |
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author | Ricardo eFernandez Gino eNardocci Cristina eNavarro Edison Pablo Reyes Edison Pablo Reyes Claudio eAcuña-Castillo Paula P Cortés Paula P Cortés |
author_facet | Ricardo eFernandez Gino eNardocci Cristina eNavarro Edison Pablo Reyes Edison Pablo Reyes Claudio eAcuña-Castillo Paula P Cortés Paula P Cortés |
author_sort | Ricardo eFernandez |
collection | DOAJ |
description | 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. |
first_indexed | 2024-12-11T18:36:27Z |
format | Article |
id | doaj.art-c4431b0adf1549ebbfb6589c6123803d |
institution | Directory Open Access Journal |
issn | 1664-042X |
language | English |
last_indexed | 2024-12-11T18:36:27Z |
publishDate | 2014-12-01 |
publisher | Frontiers Media S.A. |
record_format | Article |
series | Frontiers in Physiology |
spelling | doaj.art-c4431b0adf1549ebbfb6589c6123803d2022-12-22T00:54:45ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2014-12-01510.3389/fphys.2014.00489121047Neural reflex regulation of systemic inflammation: potential new targets for sepsis therapy.Ricardo eFernandez0Gino eNardocci1Cristina eNavarro2Edison Pablo Reyes3Edison Pablo Reyes4Claudio eAcuña-Castillo5Paula P Cortés6Paula P Cortés7Universidad Andrés BelloUniversidad Andrés BelloUniversidad Andrés BelloClínica Alemana - Universidad del DesarrolloUniversidad Autónoma de ChileUniversidad de Santiago de ChileUniversidad Andrés BelloBioAdvisingSepsis 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.http://journal.frontiersin.org/Journal/10.3389/fphys.2014.00489/fullCarotid BodySepsisVagus Nervesystemic inflammationreflex control of inflammation |
spellingShingle | Ricardo eFernandez Gino eNardocci Cristina eNavarro Edison Pablo Reyes Edison Pablo Reyes Claudio eAcuña-Castillo Paula P Cortés Paula P Cortés Neural reflex regulation of systemic inflammation: potential new targets for sepsis therapy. Frontiers in Physiology Carotid Body Sepsis Vagus Nerve systemic inflammation reflex control of inflammation |
title | Neural reflex regulation of systemic inflammation: potential new targets for sepsis therapy. |
title_full | Neural reflex regulation of systemic inflammation: potential new targets for sepsis therapy. |
title_fullStr | Neural reflex regulation of systemic inflammation: potential new targets for sepsis therapy. |
title_full_unstemmed | Neural reflex regulation of systemic inflammation: potential new targets for sepsis therapy. |
title_short | Neural reflex regulation of systemic inflammation: potential new targets for sepsis therapy. |
title_sort | neural reflex regulation of systemic inflammation potential new targets for sepsis therapy |
topic | Carotid Body Sepsis Vagus Nerve systemic inflammation reflex control of inflammation |
url | http://journal.frontiersin.org/Journal/10.3389/fphys.2014.00489/full |
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