Proteomic analysis reveals down-regulation of surfactant protein B in murine type II pneumocytes infected with influenza A virus

Lemme P. Kebaabetswe, Anoria K. Haick, Marina A. Gritsenko, Thomas L. Fillmore, Rosalie K. Chu, Samuel O. Purvine, Bobbie Jo Webb-Robertson, Melissa M. Matzke, Richard D. Smith, Katrina M. Waters, Thomas O. Metz, Tanya A. Miura

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish
Pages (from-to)96-107
Number of pages12
JournalVirology
Volume483
DOIs
Publication statusPublished - Sep 1 2015

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Alveolar Epithelial Cells
Influenza A virus
Surface-Active Agents
Proteomics
Down-Regulation
Proteins
Antigen Presentation
Mitochondrial Membranes
Virus Diseases
Infection
Cytoskeleton
Immunoblotting
Liquid Chromatography
Interferons
Energy Metabolism
Chromatin
Fluorescent Antibody Technique
Cultured Cells
Permeability
Mass Spectrometry

All Science Journal Classification (ASJC) codes

  • Virology

Cite this

Kebaabetswe, Lemme P. ; Haick, Anoria K. ; Gritsenko, Marina A. ; Fillmore, Thomas L. ; Chu, Rosalie K. ; Purvine, Samuel O. ; Webb-Robertson, Bobbie Jo ; Matzke, Melissa M. ; Smith, Richard D. ; Waters, Katrina M. ; Metz, Thomas O. ; Miura, Tanya A. / Proteomic analysis reveals down-regulation of surfactant protein B in murine type II pneumocytes infected with influenza A virus. In: Virology. 2015 ; Vol. 483. pp. 96-107.
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abstract = "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.",
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Kebaabetswe, LP, Haick, AK, Gritsenko, MA, Fillmore, TL, Chu, RK, Purvine, SO, Webb-Robertson, BJ, Matzke, MM, Smith, RD, Waters, KM, Metz, TO & Miura, TA 2015, 'Proteomic analysis reveals down-regulation of surfactant protein B in murine type II pneumocytes infected with influenza A virus', Virology, vol. 483, pp. 96-107. https://doi.org/10.1016/j.virol.2015.03.045

Proteomic analysis reveals down-regulation of surfactant protein B in murine type II pneumocytes infected with influenza A virus. / Kebaabetswe, Lemme P.; Haick, Anoria K.; Gritsenko, Marina A.; Fillmore, Thomas L.; Chu, Rosalie K.; Purvine, Samuel O.; Webb-Robertson, Bobbie Jo; Matzke, Melissa M.; Smith, Richard D.; Waters, Katrina M.; Metz, Thomas O.; Miura, Tanya A.

In: Virology, Vol. 483, 01.09.2015, p. 96-107.

Research output: Contribution to journalArticle

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AU - Kebaabetswe, Lemme P.

AU - Haick, Anoria K.

AU - Gritsenko, Marina A.

AU - Fillmore, Thomas L.

AU - Chu, Rosalie K.

AU - Purvine, Samuel O.

AU - Webb-Robertson, Bobbie Jo

AU - Matzke, Melissa M.

AU - Smith, Richard D.

AU - Waters, Katrina M.

AU - Metz, Thomas O.

AU - Miura, Tanya A.

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N2 - 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.

AB - 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.

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