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RESEARCH PRODUCT

Reduced apoptosis of CD8+ T-Lymphocytes in the airways of smokers with mild/moderate COPD

Alan L. JamesAlan L. JamesElisabetta PaceMarina SaettaLiboria SienaJohn G. ElliotMaria R. BonsignoreSimonetta BaraldoMark GjomarkajAndreina Bruno

subject

Pulmonary and Respiratory MedicineMaleapoptosis cytotoxic T-lymphocytes inflammation lung tissueInflammationApoptosisSettore MED/10 - Malattie Dell'Apparato RespiratorioCD8-Positive T-LymphocytesFEV1/FVC ratioPulmonary Disease Chronic ObstructiveSubmucosaForced Expiratory VolumeParenchymamedicineHumansLungLung tissueInflammationCOPDAnalysis of VarianceLungbusiness.industryCytotoxic T-lymphocytesSmokingMiddle Agedrespiratory systemmedicine.diseaseImmunohistochemistryrespiratory tract diseasesmedicine.anatomical_structureImmunologybehavior and behavior mechanismsFemalemedicine.symptomAirwaybusinessCD8

description

SummaryChronic obstructive pulmonary disease (COPD) is characterised by chronic inflammation in airways and lung parenchyma. CD8+ T-lymphocytes, crucial effector and regulatory cells in inflammation, are increased in the central and peripheral airways in COPD. The aim of this study was to assess the role of apoptosis in the accumulation of CD8+ T-lymphocytes within the airway wall in COPD. We examined the submucosa of transverse sections of central and peripheral airways from post-operative tissues from non-smokers (n = 16), smokers with normal lung function (n = 16), smokers with mild/moderate COPD (n = 16), and smokers with severe/very severe COPD (n = 9). TUNEL and immunohistochemistry techniques were used to identify apoptosis and cell phenotype, respectively. The percentage of apoptotic CD8+ T-lymphocytes was significantly lower (p < 0.0001) in smokers with mild/moderate COPD than in non-smokers, smokers with normal lung function, and smokers with severe/very severe COPD, and was positively related to values of FEV1 and FEV1/FVC ratio, both in central and in peripheral airways. These data suggest that reduced apoptosis of CD8+ T-lymphocytes may be an important mechanism that contributes to the accumulation of these cells in the airway submucosa in smokers with mild/moderate COPD.

10.1016/j.rmed.2011.04.014http://dx.doi.org/10.1016/j.rmed.2011.04.014