Granulocyte-Macrophage Colony Stimulating Factor As an Indirect Mediator of Nociceptor Activation and Pain.
Animals
Calcium Signaling
/ drug effects
Cell Communication
Cells, Cultured
Chronic Pain
/ chemically induced
Culture Media, Conditioned
/ pharmacology
Female
Ganglia, Spinal
/ cytology
Gene Expression Regulation
/ drug effects
Granulocyte-Macrophage Colony-Stimulating Factor
/ physiology
Inflammation
/ chemically induced
MAP Kinase Signaling System
/ drug effects
Macrophages
/ drug effects
Male
Mice
Mice, Inbred C57BL
Nerve Growth Factor
/ pharmacology
Nociceptors
/ drug effects
Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
/ drug effects
STAT5 Transcription Factor
/ physiology
Sensory Receptor Cells
/ drug effects
Transcription, Genetic
/ drug effects
GM-CSF
chronic pain
neuroimmune interaction
Journal
The Journal of neuroscience : the official journal of the Society for Neuroscience
ISSN: 1529-2401
Titre abrégé: J Neurosci
Pays: United States
ID NLM: 8102140
Informations de publication
Date de publication:
11 03 2020
11 03 2020
Historique:
received:
16
09
2019
revised:
07
01
2020
accepted:
14
01
2020
pubmed:
6
2
2020
medline:
9
9
2020
entrez:
6
2
2020
Statut:
ppublish
Résumé
The interaction between the immune system and the nervous system has been at the center of multiple research studies in recent years. Whereas the role played by cytokines as neuronal mediators is no longer contested, the mechanisms by which cytokines modulate pain processing remain to be elucidated. In this study, we have analyzed the involvement of granulocyte-macrophage colony stimulating factor (GM-CSF) in nociceptor activation in male and female mice. Previous studies have suggested GM-CSF might directly activate neurons. However, here we established the absence of a functional GM-CSF receptor in murine nociceptors, and suggest an indirect mechanism of action, via immune cells. We report that GM-CSF applied directly to magnetically purified nociceptors does not induce any transcriptional changes in nociceptive genes. In contrast, conditioned medium from GM-CSF-treated murine macrophages was able to drive nociceptor transcription. We also found that conditioned medium from nociceptors treated with the well established pain mediator, nerve growth factor, could also modify macrophage gene transcription, providing further evidence for a bidirectional crosstalk.
Identifiants
pubmed: 32019828
pii: JNEUROSCI.2268-19.2020
doi: 10.1523/JNEUROSCI.2268-19.2020
pmc: PMC7083288
doi:
Substances chimiques
Culture Media, Conditioned
0
Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
0
STAT5 Transcription Factor
0
Granulocyte-Macrophage Colony-Stimulating Factor
83869-56-1
Nerve Growth Factor
9061-61-4
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2189-2199Subventions
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : NIDDK NIH HHS
ID : R01 DK118971
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS102722
Pays : United States
Organisme : Wellcome Trust
ID : 1043147
Pays : United Kingdom
Informations de copyright
Copyright © 2020 the authors.
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