Abstract

Chronic obstructive pulmonary disease (COPD) is caused by exposure to toxic gases and particles, most often cigarette smoke, leading to septal tissue damage, remodeling of small airways, airway obstruction, and a subsequent decline in lung function. The disease pathogenesis is related to an abnormal smoke-induced and antigen-driven inflammatory response of the lungs involving innate and specific immune cells. In this study, we characterized the dynamics of inflammatory cell recruitment after chronic cigarette smoke (CS) exposure in a COPD mouse model and focused on adaptive and innate immune cells.

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