A basic solution to activate the cholinergic anti-inflammatory pathway via the mesothelium?
Macrophage polarization
Perisplenitis
Sodium bicarbonate
Tumor-necrosis factor
Vagal nerve stimulation
Journal
Pharmacological research
ISSN: 1096-1186
Titre abrégé: Pharmacol Res
Pays: Netherlands
ID NLM: 8907422
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
11
10
2018
revised:
20
12
2018
accepted:
03
01
2019
pubmed:
8
1
2019
medline:
4
9
2019
entrez:
8
1
2019
Statut:
ppublish
Résumé
Much research now indicates that vagal nerve stimulation results in a systemic reduction in inflammatory cytokine production and an increase in anti-inflammatory cell populations that originates from the spleen. Termed the 'cholinergic anti-inflammatory pathway', therapeutic activation of this innate physiological response holds enormous promise for the treatment of inflammatory disease. Much controversy remains however, regarding the underlying physiological pathways mediating this response. This controversy is anchored in the fact that the vagal nerve itself does not innervate the spleen. Recent research from our own laboratory indicating that oral intake of sodium bicarbonate stimulates splenic anti-inflammatory pathways, and that this effect may require transmission of signals to the spleen through the mesothelium, provide new insight into the physiological pathways mediating the cholinergic anti-inflammatory pathway. In this review, we examine proposed models of the cholinergic anti-inflammatory pathway and attempt to frame our recent results in relation to these hypotheses. Following this discussion, we then provide an alternative model of the cholinergic anti-inflammatory pathway which is consistent both with our recent findings and the published literature. We then discuss experimental approaches that may be useful to delineate these hypotheses. We believe the outcome of these experiments will be critical in identifying the most appropriate methods to harness the therapeutic potential of the cholinergic anti-inflammatory pathway for the treatment of disease and may also shed light on the etiology of other pathologies, such as idiopathic fibrosis.
Identifiants
pubmed: 30616018
pii: S1043-6618(18)31568-8
doi: 10.1016/j.phrs.2019.01.007
pmc: PMC6391187
mid: NIHMS1518627
pii:
doi:
Substances chimiques
Acetylcholine
N9YNS0M02X
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
236-248Subventions
Organisme : NHLBI NIH HHS
ID : P01 HL134604
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK099548
Pays : United States
Informations de copyright
Copyright © 2019 Elsevier Ltd. All rights reserved.
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