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Susceptibility to influenza virus infection of bronchial biopsies in asthma  Ben Nicholas, PhD, Sarah Dudley, PhD, Kamran Tariq, MD, Peter Howarth, DM,

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Presentation on theme: "Susceptibility to influenza virus infection of bronchial biopsies in asthma  Ben Nicholas, PhD, Sarah Dudley, PhD, Kamran Tariq, MD, Peter Howarth, DM,"— Presentation transcript:

1 Susceptibility to influenza virus infection of bronchial biopsies in asthma 
Ben Nicholas, PhD, Sarah Dudley, PhD, Kamran Tariq, MD, Peter Howarth, DM, Kerry Lunn, BSc, Sandy Pink, BA, Peter J. Sterk, PhD, Ian M. Adcock, PhD, Phillip Monk, PhD, Ratko Djukanović, MD  Journal of Allergy and Clinical Immunology  Volume 140, Issue 1, Pages e4 (July 2017) DOI: /j.jaci Copyright © 2017 American Academy of Allergy, Asthma & Immunology Terms and Conditions

2 Fig 1 Comparison of bronchial biopsies from healthy subjects and subjects with asthma following influenza virus exposure. A, Effects on (i) epithelial cell infection and (ii) viral shedding. B, Fold change in MHC class II cell surface expression on (i) T lymphocytes and (ii) epithelial cells. C, Mediator secretion from infected biopsies. N = 10 per group compared using Mann-Whitney test. MCP, Monocyte chemoattractant protein; MIP, macrophage inflammatory protein; NP, Influenza A virus nucleoprotein. *P < .05, **P < .005, and ***P < .001. Journal of Allergy and Clinical Immunology  , e4DOI: ( /j.jaci ) Copyright © 2017 American Academy of Allergy, Asthma & Immunology Terms and Conditions

3 Fig 2 A, Effect of addition of exogenous corticosteroid to bronchial explants from healthy subjects on (i) epithelial cell infection and (ii) viral shedding. B, Fold change in MHC class II cell surface expression following infection on the cell surface of (i) T lymphocytes and (ii) epithelial cells. C, Mediator secretion from infected biopsies. N = 10 per group. Data were compared using Wilcoxon matched pairs signed rank test. MCP, Monocyte chemoattractant protein; MIP, macrophage inflammatory protein; NP, Influenza A virus nucleoprotein. *P < .05, **P < .005, and ***P < .001. Journal of Allergy and Clinical Immunology  , e4DOI: ( /j.jaci ) Copyright © 2017 American Academy of Allergy, Asthma & Immunology Terms and Conditions

4 Fig E1 Leukocytes and epithelial cells dispersed from bronchial biopsies were phenotypically identified by flow cytometry. A, Gating strategy: (i) Size using forward scatter properties, (ii) CD45-PE/CF594 to identify leukocytes, (iii) CD3-PECy7 on the CD45+ cell population to identify T lymphocytes, and (iv) CD326-PerCPCy5.5 on the CD45- population to identify epithelial cells. B, Quantification of epithelial cell influenza infection within bronchial biopsies by flow cytometric detection of influenza viral nucleoprotein (NP-FITC) in infected biopsies compared with mock-infected control explants. C, Viral dose- response curve performed in resected lung tissue explants. D, HLA-DR (MHC class II) expression on the surface of T lymphocytes and epithelial cells (HLA-DR-APCCy7) with isotype control used to subtract from positive stains to calculate the sMFI. APC, Antigen-presenting cell; FITC, fluorescein isothiocyanate; IFV, influenza virus; PE, phycoerythrin. Journal of Allergy and Clinical Immunology  , e4DOI: ( /j.jaci ) Copyright © 2017 American Academy of Allergy, Asthma & Immunology Terms and Conditions

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