Research Papers: Gerotarget (Focus on Aging):
Inflammaging increases susceptibility to cigarette smoke-induced COPD
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Gerrit John-Schuster1, Stefanie Günter1, Katrin Hager1, Thomas M. Conlon1, Oliver Eickelberg1,2, Ali Önder Yildirim1
1Comprehensive Pneumology Center, Institute of Lung Biology and Disease, Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), 85764 Neuherberg, Germany
2Klinikum der Universität München, 81377 München, Germany
Gerrit John-Schuster, email: email@example.com
Ali Önder Yildirim, email: firstname.lastname@example.org
Keywords: aging, B cells, iBALT, COPD, cigarette smoke, Gerotarget
Received: March 3, 2015 Accepted: May 6, 2015 Published: May 24, 2015
Chronic obstructive pulmonary disease (COPD) is related to an abnormal chronic inflammatory response of the lung to mainly cigarette smoke (CS) and the disease risk is increased in aged individuals. The source of this chronic inflammation is due to the repeated and progressive activation of immune cells. We hypothesize that in a chronic CS-induced mouse model, the predisposition to COPD pathogenesis in aged mice is characterized by an elevated immune response compared to young animals. We measured several characteristics of COPD in young and old mice (2 and 12 months of age) exposed to CS for 3 months. CS-exposed aged mice exhibited increased lung compliance (0.061 ± 0.008 vs. 0.055 ± 0.006 ml/cm H2O, p < 0.01), emphysema development (35.36 ± 0.71 vs. 25.31 ± 0.005 μm; p < 0.01) and airway remodeling (2.15 ± 0.37 vs. 1.09 ± 0.64 μm3/μm2; p < 0.01) compared to control animals, which was not seen in CS-exposed young mice. Quantification of lung tissue inflammation revealed a significantly greater volume of inducible bronchus-associated lymphoid tissue structures in aged mice after CS exposure (5.94 ± 2.89 vs. 2.37 ± 1.69 μm3/μm2; p < 0.01). Our results indicate that age-induced lung inflammation is further elevated after CS exposure in old mice, potentially via an age-induced change in immune cell susceptibility to CS thereby accelerating the pathophysiological hallmarks of COPD.
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