Abstract
Asthma and COPD are chronic obstructive diseases with a certain degree of physiologic and pathologic similarities and the Dutch Hypothesis proposes that these diseases could be phenotypes of the same process. This hypothesis has never been universally accepted due to the evident differences between the two diseases. However COPD has two distinct pathological phenotypes, Panlobular Emphysema (PLE) where airflow obstruction is secondary to loss of elasticity and Centrilobular Emphysema (CLE) where airflow obstruction is secondary to bronchiolar remodeling with increased muscle and smaller diameter. We hypothesize that CLE could have features of Asthma different from PLE, especially as far as mast cells (MC) inflammation and their relation to airway reactivity. Therefore, we quantified tryptase stained MC in all layers (submucosa, smooth muscle and adventitia) of small airways in 27 lungs with CLE, 24 with PLE, 8 smokers without emphysema (SNE) and 8 non smokers (NS). MC in smooth muscle of small airways were significantly higher in CLE (206±41 cells/mm2) than in PLE (104±21 cells/mm2; p=0.01), SNE (107±54 cells/mm2; p=0.05) and NS (105±27 cells/mm2; p=0.05). Moreover, the degree of MC infiltration in the smooth muscle was related with the degree of hyperresponsiveness, as it has been shown in Asthma (PC20<3mg/ml: 396±116 cells/mm2, PC20 3-8mg/ml: 89±69 cells/mm2 and PC20>8mg/ml: 107±21 cells/mm2; p=0.02 for all). In conclusion, MC infiltration of the muscle layer and its relation to airway reactivity, an important mechanism in the pathogenesis of Asthma, is a prominent feature of COPD patients with CLE, but not with PLE. These findings suggest that CLE could be the COPD link to the Dutch Hypothesis.
- © 2011 ERS
