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Sci Rep. 2018 Jul 9;8(1):10340. doi: 10.1038/s41598-018-28655-9.

Unique Lipid Signatures of Extracellular Vesicles from the Airways of Asthmatics.

Author information

1
Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
2
Department of Pharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, AL, USA.
3
Targeted Metabolomics and Proteomics Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA.
4
Center for AIDS Research, University of Alabama at Birmingham, Birmingham, AL, USA.
5
Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL, USA.
6
Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL, USA. jessydeshane@uabmc.edu.

Abstract

Asthma is a chronic inflammatory disease process involving the conductive airways of the human lung. The dysregulated inflammatory response in this disease process may involve multiple cell-cell interactions mediated by signaling molecules, including lipid mediators. Extracellular vesicles (EVs) are lipid membrane particles that are now recognized as critical mediators of cell-cell communication. Here, we compared the lipid composition and presence of specific lipid mediators in airway EVs purified from the bronchoalveolar lavage (BAL) fluid of healthy controls and asthmatic subjects with and without second-hand smoke (SHS) exposure. Airway exosome concentrations were increased in asthmatics, and correlated with blood eosinophilia and serum IgE levels. Frequencies of HLA-DR+ and CD54+ exosomes were also significantly higher in asthmatics. Lipidomics analysis revealed that phosphatidylglycerol, ceramide-phosphates, and ceramides were significantly reduced in exosomes from asthmatics compared to the non-exposed control groups. Sphingomyelin 34:1 was more abundant in exosomes of SHS-exposed asthmatics compared to healthy controls. Our results suggest that chronic airway inflammation may be driven by alterations in the composition of lipid mediators within airway EVs of human subjects with asthma.

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