Vagus nerve regulates the phagocytic and secretory activity of resident macrophages in the liver.
Cholinergic signaling
Kupffer cells
Liver
Phagocytosis
Vagus nerve
Journal
Brain, behavior, and immunity
ISSN: 1090-2139
Titre abrégé: Brain Behav Immun
Pays: Netherlands
ID NLM: 8800478
Informations de publication
Date de publication:
10 2019
10 2019
Historique:
received:
18
12
2018
revised:
24
06
2019
accepted:
26
06
2019
pubmed:
5
7
2019
medline:
15
8
2020
entrez:
5
7
2019
Statut:
ppublish
Résumé
The gastrointestinal (GI) tract harbors commensal microorganisms as well as invasive bacteria, toxins and other pathogens and, therefore, plays a pivotal barrier and immunological role against pathogenic agents. The vagus nerve is an important regulator of the GI tract-associated immune system, having profound effects on inflammatory responses. Among GI tract organs, the liver is a key site of immune surveillance, as it has a large population of resident macrophages and receives the blood drained from the guts through the hepatic portal circulation. Although it is widely accepted that the hepatic tissue is a major target for vagus nerve fibers, the role of this neural circuit in liver immune functions is still poorly understood. Herein we used in vivo imaging techniques, including confocal microscopy and scintigraphy, to show that vagus nerve stimulation increases the phagocytosis activity by resident macrophages in the liver, even on the absence of an immune challenge. The activation of this neural circuit in a non-lethal model of sepsis optimized the removal of bacteria in the liver and resulted in the production of anti-inflammatory and pro-regenerative cytokines. Our findings provide new insights into the neural regulation of the immune system in the liver.
Identifiants
pubmed: 31271871
pii: S0889-1591(18)31225-X
doi: 10.1016/j.bbi.2019.06.041
pmc: PMC7826199
mid: NIHMS1660688
pii:
doi:
Substances chimiques
Cytokines
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
444-454Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK116004
Pays : United States
Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.
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