Biomedical Engineering Reference
In-Depth Information
2
Inflammation in Lung Parenchyma
Graziella Turato, Simonetta Baraldo, Elisabetta Balestro,
Renzo Zuin, and Marina Saetta
Department of Clinical and Experimental Medicine, Section of Respiratory
Diseases, University of Padova, Padova, Italy
I.
INTRODUCTION
Airflow obstruction is the functional consequence of pathological changes
induced by cigarette smoking in peripheral airways and lung parenchyma.
These include both inflammatory and structural changes, mainly airway
remodeling and parenchymal destruction (which characterizes emphysema).
Airway remodeling and inflammation will contribute to airflow obstruction
by promoting airway narrowing and lumen occlusion, while parenchymal
destruction will contribute to airflow obstruction by reducing the elastic
recoil of the lung as well as by destroying alveolar attachments and thereby
reducing the elastic load applied to the airways (1,2). Whether airflow
obstruction is always caused by emphysema or whether a disease of the con-
ducting airways without emphysema could also cause airflow obstruction is
still uncertain. Furthermore, it has been reported that smokers may develop
emphysema even in the presence of normal lung function (3,4). These facts
highlight the complexity of Chronic Obstructive Pulmonary Disease
(COPD) and particularly of the relationship among airway pathology,
emphysema, and airflow obstruction.
The role of mucus hypersecretion in COPD is even more debated. Tra-
ditionally, mucus hypersecretion has been considered irrelevant to the devel-
opment of chronic airflow obstruction in smokers (5,6). On the other hand,
the observation that chronic sputum production was associated with both
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