Inflammation gives rise to the release of oxidants and elastolytic agents that can damage the alveolar walls. Lung tissue has regenerative capacity, and fiber renewal is possible, however, connective tissue turnover is a complex issue. For example, the enormous damage caused by pneumonia can heal with time. However when damage is recurring or chronic such as in cigarette smokers, or the elastase inhibiting power is reduced (as is seen in either cigarette smokers or patients with α1-antitrypsin (AAT) deficiency), alveolar damage is progressive leading to pulmonary
AAT substitution therapy in deficient (non-smoking!!!) individuals may lead to a slowing down of this process and this expensive therapy is applied in several countries, especially the USA. However the evidence that it really helps is poor so far.
The opposite in disturbing the balance of connective tissue turnover is fibrosis, for which so far no cure is available. An international trial is being conducted to evaluate the anti-oxidant protective effect of N-acetylcysteine, which is a radical scavenger next to a mucolytic, in pulmonary fibrosis.
α1-antitrypsin protects the alveoli from elastase activity.
Extra info: Close In the conditions of smoking and α1-antitrypsin deficiency, the alveoli are not protected, resulting in chronic lung disease.
Alveolar damage can result from oxidant or elastolytic activity.
Extra info: Inflammation causes alveolar damage through its release of oxidants and elastolytic activity.