Pneumologie 2011; 65 - A26
DOI: 10.1055/s-0031-1296117

Dynamics of inflammatory cell recruitment in a cigarette smoke induced COPD mouse model

K Kohse 1, G John 1, O Eickelberg 1, 2, AÖ Yildirim 1
  • 1Comprehensive Pneumology Center, Institute of Lung Biology and Disease
  • 2Institute of Experimental Pneumology, Klinikum der Universität München, Helmholtz Zentrum München

Introduction: Chronic obstructive pulmonary disease (COPD) is characterized by septal tissue damage, remodeling of small airways, airway obstruction, and a subsequent decline in lung function. The disease pathogenesis is related to an abnormal inflammatory response of the lungs to toxic gases and particles, most often cigarette smoke, and increasing evidence suggests that innate (neutrophils and macrophages) and specific immune cells (T and B lymphocytes) are involved in lung tissue damage in COPD (Barnes 2008; Hogg et al. 2004). In this study, we characterized the dynamics of inflammatory cell recruitment after sub-acute cigarette smoke exposure in a COPD mouse model.

Methods: Female C57BL/6 mice were exposed to a cigarette smoke-concentration of 500mg/m3 total particulate matter for 50 minutes twice a day for 3, 7, 14 and 28 days. Animals were sacrificed and analyzed 24h after the last exposure. Control animals were kept in a filtered air environment. Broncho-alveolar lavage fluid was obtained to perform differenzial cell counts and lung tissue was used to determine lymphocyte distribution by flow cytometry (FACS).

Results: Compared to filtered air control animals, cigarette smoke exposed mice showed significantly increased total BAL cell counts, due to elevated numbers of neutrophils and macrophages. After 14 days of smoke exposure BAL lymphocyte levels started to increase, an effect that was even more significant after 28 days. By FACS analysis of lung tissue we could confirm that CD4+ and CD8+ T cells are involved in the inflammatory response to cigarette smoke.

Conclusion: These results demonstrate a time dependent recruitment of inflammatory cells in a cigarette smoke-induced mouse model. These initial inflammatory processes might contribute to COPD pathogenesis at an early stage of smoke exposure. A long-term COPD mouse model will be useful to investigate the relation between inflammatory cell recruitment and the development of COPD.