Phospholipase Cε plays a crucial role in neutrophilic inflammation accompanying acute lung injury through augmentation of CXC chemokine production from alveolar epithelial cells.
Acute lung injury
Acute respiratory distress syndrome
Alveolar epithelial cells
Cxcl5
Inflammation
Mouse model
Neutrophil
Nuclear factor-κB
Phospholipase Cε
Journal
Respiratory research
ISSN: 1465-993X
Titre abrégé: Respir Res
Pays: England
ID NLM: 101090633
Informations de publication
Date de publication:
11 Jan 2019
11 Jan 2019
Historique:
received:
07
10
2018
accepted:
02
01
2019
entrez:
13
1
2019
pubmed:
13
1
2019
medline:
12
3
2019
Statut:
epublish
Résumé
We have shown that phospholipase Cε (PLCε), an effector of Ras and Rap1 small GTPases, plays pivotal roles in inflammation and inflammation-associated carcinogenesis by augmenting proinflammatory cytokine production from epithelial cells of various organs. The purpose of this study is to analyze its role in neutrophilic alveolar inflammation accompanying acute lung injury (ALI), focusing on that in alveolar epithelial cells (AECs), which are known to make a major contribution to the pathogenesis of ALI. We examine the effect of the PLCε genotypes on the development of ALI induced by intratracheal administration of lipopolysaccharide (LPS) to PLCε wild-type (PLCε Compared to PLCε PLCε-mediated augmentation of the production of the CXC family of chemokines, in particular Cxcl5, in AECs plays a crucial role in neutrophilic alveolar inflammation accompanying ALI, suggesting that PLCε may be a potential molecular target for the treatment of acute respiratory distress syndrome.
Sections du résumé
BACKGROUND
BACKGROUND
We have shown that phospholipase Cε (PLCε), an effector of Ras and Rap1 small GTPases, plays pivotal roles in inflammation and inflammation-associated carcinogenesis by augmenting proinflammatory cytokine production from epithelial cells of various organs. The purpose of this study is to analyze its role in neutrophilic alveolar inflammation accompanying acute lung injury (ALI), focusing on that in alveolar epithelial cells (AECs), which are known to make a major contribution to the pathogenesis of ALI.
METHODS
METHODS
We examine the effect of the PLCε genotypes on the development of ALI induced by intratracheal administration of lipopolysaccharide (LPS) to PLCε wild-type (PLCε
RESULTS
RESULTS
Compared to PLCε
CONCLUSIONS
CONCLUSIONS
PLCε-mediated augmentation of the production of the CXC family of chemokines, in particular Cxcl5, in AECs plays a crucial role in neutrophilic alveolar inflammation accompanying ALI, suggesting that PLCε may be a potential molecular target for the treatment of acute respiratory distress syndrome.
Identifiants
pubmed: 30634975
doi: 10.1186/s12931-019-0975-4
pii: 10.1186/s12931-019-0975-4
pmc: PMC6330467
doi:
Substances chimiques
Chemokine CXCL5
0
Cxcl5 protein, mouse
0
Lipopolysaccharides
0
Phosphoinositide Phospholipase C
EC 3.1.4.11
phospholipase C epsilon
EC 3.1.4.11
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
9Subventions
Organisme : JSPS KAKENHI
ID : 26461188
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