tetano
Editor, Senior Moderator
Virology. 2015 May 8;483:96-107. doi: 10.1016/j.virol.2015.03.045. [Epub ahead of print]
[h=1]Proteomic analysis reveals down-regulation of surfactant protein B in murine type II pneumocytes infected with influenza A virus.[/h] Kebaabetswe LP[SUP]1[/SUP], Haick AK[SUP]1[/SUP], Gritsenko MA[SUP]2[/SUP], Fillmore TL[SUP]3[/SUP], Chu RK[SUP]3[/SUP], Purvine SO[SUP]3[/SUP], Webb-Robertson BJ[SUP]4[/SUP], Matzke MM[SUP]2[/SUP], Smith RD[SUP]2[/SUP], Waters KM[SUP]2[/SUP], Metz TO[SUP]2[/SUP], Miura TA[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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 Pisis isiiiR8-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.
[h=4]KEYWORDS:[/h] Influenza A virus; Primary alveolar type II epithelial cells; Quantitative proteomics; Surfactant protein B
PMID: 25965799 [PubMed - as supplied by publisher]
[h=1]Proteomic analysis reveals down-regulation of surfactant protein B in murine type II pneumocytes infected with influenza A virus.[/h] Kebaabetswe LP[SUP]1[/SUP], Haick AK[SUP]1[/SUP], Gritsenko MA[SUP]2[/SUP], Fillmore TL[SUP]3[/SUP], Chu RK[SUP]3[/SUP], Purvine SO[SUP]3[/SUP], Webb-Robertson BJ[SUP]4[/SUP], Matzke MM[SUP]2[/SUP], Smith RD[SUP]2[/SUP], Waters KM[SUP]2[/SUP], Metz TO[SUP]2[/SUP], Miura TA[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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 Pisis isiiiR8-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.
[h=4]KEYWORDS:[/h] Influenza A virus; Primary alveolar type II epithelial cells; Quantitative proteomics; Surfactant protein B
PMID: 25965799 [PubMed - as supplied by publisher]