Lipidomic Profiling of Bronchoalveolar Lavage Fluid Extracellular Vesicles Indicates Their Involvement in Lipopolysaccharide-Induced Acute Lung Injury.
Acute lung injury
Extracellular vesicles
Inflammation
Macrophage
Polyunsaturated fatty acids
Journal
Journal of innate immunity
ISSN: 1662-8128
Titre abrégé: J Innate Immun
Pays: Switzerland
ID NLM: 101469471
Informations de publication
Date de publication:
2022
2022
Historique:
received:
27
10
2021
accepted:
13
01
2022
pubmed:
4
4
2022
medline:
9
9
2022
entrez:
3
4
2022
Statut:
ppublish
Résumé
Emerging data support the pivotal role of extracellular vesicles (EVs) in normal cellular physiology and disease conditions. However, despite their abundance, there is much less information about the lipid mediators carried in EVs, especially in the context of acute lung injury (ALI). Our data demonstrate that C57BL/6 mice subjected to intranasal Escherichia coli lipopolysaccharide (LPS)-induced ALI release, a higher number of EVs into the alveolar space, compared to saline-treated controls. EVs released during ALI originated from alveolar epithelial cells, macrophages, and neutrophils and carry a diverse array of lipid mediators derived from ω-3 and ω-6 polyunsaturated fatty acids (PUFA). The eicosanoids in EVs correlated with cellular levels of arachidonic acid, expression of cytosolic phospholipase A2, cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome epoxygenase p450 proteins in pulmonary macrophages. Furthermore, EVs from LPS-toll-like receptor 4 knockout (TLR4-/-) mice contained significantly lower amounts of COX and LOX catalyzed eicosanoids and ω-3 PUFA metabolites. More importantly, EVs from LPS-treated wild-type mice increased TNF-α release by macrophages and reduced alveolar epithelial monolayer barrier integrity compared to EVs from LPS-treated TLR4-/- mice. In summary, our study demonstrates for the first time that the EV carried PUFA metabolite profile in part depends on the inflammatory status of the lung macrophages and modulates pulmonary macrophage and alveolar epithelial cell function during LPS-induced ALI.
Identifiants
pubmed: 35367992
pii: 000522338
doi: 10.1159/000522338
pmc: PMC9485986
doi:
Substances chimiques
Lipopolysaccharides
0
Toll-Like Receptor 4
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
555-568Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL137224
Pays : United States
Informations de copyright
© 2022 The Author(s). Published by S. Karger AG, Basel.
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