Abstract

BackgroundInflammation of the airways is present in COPD with increased number of inflammatory cells including killer cells that lyse their target cells by two mechanisms; membranolysis in which secreted molecules such as granzymes form pores in the membrane of target cells; and apoptosis. Granzyme B has the strongest apoptotic activity of all granzymes. Aim of this workAim of this work was to study the relation between Granzyme B, tobacco smoking and chronic obstructive pulmonary disease. MethodsThe study included 40 clinically stable COPD patients classified according to GOLD (2013) criteria into two groups; moderate (GOLD II) and severe (GOLD III) plus 40 apparently healthy control subjects (20 smokers and 20 nonsmokers). Pulmonary function results and serum levels of Granzyme B (measured by ELISA) were recorded. ResultsGranzyme B levels are elevated in COPD. Cigarette smoking appears to be a direct stimulus to Granzyme B production. Granzyme B could play a role in the pathogenesis of COPD. Aging seems to be a risk factor for Granzyme B production and pathogenesis of COPD. ConclusionGranzyme B levels are elevated in COPD. Cigarette smoking appears to be a direct stimulus to Granzyme B production. Granzyme B could play a role in the pathogenesis of COPD. Aging seems to be a risk factor for Granzyme B production and pathogenesis of COPD.

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