Increased phosphorylated p38 mitogenactivated protein kinase in COPD lungs

Kate Gaffey, Sophie Reynolds, Jonathan Plumb, Manminder Kaur, Dave Singh

    Research output: Contribution to journalArticlepeer-review


    The p38 mitogen-activated protein kinase (MAPK) pathway is upregulated in chronic obstructive pulmonary disease (COPD). To date, dual labelling to identify cell-type-specific presence of phosphorylated (phospho-)p38 MAPK has not been carried out. Phospho-p38 MAPK was quantified in a variety of cell types in the lung tissue of 20 COPD patients, 12 smokers and 12 nonsmokers using immunohistochemistry. Paired blood and sputum neutrophils (from seven subjects with COPD), and CD8 and epithelial cells (from three subjects with COPD) were cultured with a p38 MAPK inhibitor. Supernatant tumour necrosis factor-a and CXCL8 levels were analysed by ELISA. Sputum and blood neutrophil cytospins were analysed for phospho-p38 MAPK. Phospho-p38 MAPK was increased in bronchial epithelial cells, macrophages and CD20+ and CD8+ lymphocytes in COPD lungs. Sputum and lung tissue neutrophils were devoid of phospho-p38 in all patient groups. The p38 MAPK inhibitor SB100 attenuated pro-inflammatory mediator release in COPD lung CD8 cells and airway epithelia, but there was no effect on COPD sputum neutrophils. Our data indicate cell-specific anti-inflammatory effects of p38 MAPK inhibition in the lung. Copyright © ERS 2013.
    Original languageEnglish
    Pages (from-to)28-41
    Number of pages13
    JournalEuropean Respiratory Journal
    Issue number1
    Publication statusPublished - 1 Jul 2013


    Dive into the research topics of 'Increased phosphorylated p38 mitogenactivated protein kinase in COPD lungs'. Together they form a unique fingerprint.

    Cite this