Pneumologie 2011; 65 - A51
DOI: 10.1055/s-0031-1296142

Role of Bronchial Epithelial Cells in Pathogenesis of COPD

S Rim 1, S Jahan 1, G John 1, K Kohse 1, A Bohla 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 chronic bronchitis and emphysema. Inflammation is believed to play a central role in pathogenesis of COPD. A cigarette smoke (CS) induced inflammatory reaction in bronchial airway is involved at every stage of COPD development (Hogg, NEJM 2004). Bronchioles are specifically prone to injury by CS due to abundance of Clara cells that can metabolize naphthalene (a smoke particle) by the cytochrome P450 monooxygenase system (Yildirim, ERS 2008). Our hypothesis is naphthalene-induced site selective injury of Clara cells modulates inflammatory response caused by cigarette smoke in mouse model of COPD. For this purpose we used a prior exposure of naphthalene (NA) to injure Clara cells. The question is whether prior injury with naphthalene alters cigarette smoke induced- inflammation.

Methods: C57BL/6 mice were injected with 200mg/kg body weight of naphthalene dissolved in corn oil. After day 7 and day 10, they were exposed to cigarette smoke for 3 days (500mg/m3; 2X50min/day). Differenzial cell count from the BAL fluid was performed.

Results: BAL count showed day 7–14 as the persistent inflammatory period after naphthalene injection though the inflammation caused by naphthalene was minor at tissue level. But naphthalene pre-treatment showed increase of inflammatory cells induced by cigarette smoke at BAL level.

Conclusion: Naphthalene induces time dependent exfoliation of Clara cells. Exposure with naphthalene and cigarette smoke shows higher neutrophilic accumulation in BAL indicating that the bronchial epithelial cells contribute to control the inflammation induced by smoke. Further investigation will be carried out to characterize the inflammatory markers and their interaction with Clara cell.