Proteomic analysis reveals down-regulation of surfactant protein B in murine type II pneumocytes infected with influenza A virus.
Autor: | Kebaabetswe LP; Department of Biological Sciences, University of Idaho, Moscow, ID 83844, USA., Haick AK; Department of Biological Sciences, University of Idaho, Moscow, ID 83844, USA., Gritsenko MA; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352, USA., Fillmore TL; Environmental Molecular Sciences Laboratory, Pacific Northwest National Laboratory, Richland, WA 99352, USA., Chu RK; Environmental Molecular Sciences Laboratory, Pacific Northwest National Laboratory, Richland, WA 99352, USA., Purvine SO; Environmental Molecular Sciences Laboratory, Pacific Northwest National Laboratory, Richland, WA 99352, USA., Webb-Robertson BJ; Computational and Statistical Analytics Division, Pacific Northwest National Laboratory, Richland, WA 99352, USA., Matzke MM; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352, USA., Smith RD; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352, USA., Waters KM; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352, USA., Metz TO; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352, USA., Miura TA; Department of Biological Sciences, University of Idaho, Moscow, ID 83844, USA. Electronic address: tmiura@uidaho.edu. |
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Jazyk: | angličtina |
Zdroj: | Virology [Virology] 2015 Sep; Vol. 483, pp. 96-107. Date of Electronic Publication: 2015 May 15. |
DOI: | 10.1016/j.virol.2015.03.045 |
Abstrakt: | Infection of type II alveolar epithelial (ATII) cells by influenza A viruses (IAV) correlates with severe respiratory disease in humans and mice. To understand pathogenic mechanisms during IAV infection of ATII cells, murine ATII cells were cultured to maintain a differentiated phenotype, infected with IAV-PR8, which causes severe lung pathology in mice, and proteomics analyses were performed using liquid chromatography-mass spectrometry. PR8 infection increased levels of proteins involved in interferon signaling, antigen presentation, and cytoskeleton regulation. Proteins involved in mitochondrial membrane permeability, energy metabolism, and chromatin formation had reduced levels in PR8-infected cells. Phenotypic markers of ATII cells in vivo were identified, confirming the differentiation status of the cultures. Surfactant protein B had decreased levels in PR8-infected cells, which was confirmed by immunoblotting and immunofluorescence assays. Analysis of ATII cell protein profiles will elucidate cellular processes in IAV pathogenesis, which may provide insight into potential therapies to modulate disease severity. (Copyright © 2015 Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
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