Neutrophils and emphysema

Article Abstract:

A report that cigarette smoking results in the pooling of certain white blood cells, neutrophils, within the lungs of the smokers strengthens the association between neutrophils and the etiology of emphysema in tobacco smokers. Evidence from other sources indicates that protein-breaking enzymes placed in the lungs of animals can break down the elastic elements (such as the protein elastin) in tissues under certain conditions. Cigarette smoking may cause the release of an enzyme, elastase, capable of breaking down elastin in areas deep within the lungs where emphysema develops. It is likely that the chronic inflammatory process which often occurs in these patients is mediated through neutrophils and other scavenger cells, macrophages, which are the likely source of elastase. Although there is documentation on the accumulation of these cells within the lungs of active smokers, there remains no confirmed correlation between smoking, cell content and level of functional elastase activity in the lung. A system of antiproteinases has also been discovered in the lung which may counteract at least some of the elastase activity which is stimulated by smoking. Deleterious effects of smoking on the ability of the lungs to restore elastin that has been damaged is also suspected. It is likely that not all important destructive effects of smoking are known and future efforts to discover the causes of emphysema may lead to a therapy. The absence of a good laboratory method of measuring the enzyme-induced damage to the lungs from cigarette smoking remains an impediment to research.

editorial

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The effect of cigarette smoking on neutrophil kinetics in human lungs

Article Abstract:

Neutrophils are a type of white blood cell involved in the removal of debris from the bloodstream. As elements of the blood, they are generally thought of as being in constant circulation, but research has shown that a significant number of them, perhaps as many as 50 percent, attach themselves to the walls of blood vessels and constitute a "marginated pool" of neutrophils. Marginated cells can rapidly reenter the circulation if needed. Recently neutrophils have been implicated as a possible cause of a form of emphysema associated with cigarette smoking, where marginated neutrophils may be found in a 100-fold concentration as compared to erythrocytes. Radioisotope labeling was used to study the process of neutrophil concentration (retention) and subsequent washout from the lungs of nonsmokers, smokers who restrained from smoking, and current smokers. There were no statistical differences between individuals who were not currently smoking with regard to retention and washout; however, active smokers experienced a statistically significant reduction in the rate of washout of marginated neutrophils from their lungs. Smoking also caused an elevation in the number of neutrophils collecting within their lungs. These data strongly suggest that cigarette smoke increases the size of the marginated pool within the lung, suggesting the possibility that emphysema among smokers is caused by this accumulation within the small capillaries of the lungs.

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High-dose acetylcysteine in idiopathic pulmonary fibrosis

Article Abstract:

A double blind, randomized, placebo-controlled multicenter study was conducted that assessed the effectiveness over one year of a high oral dose of acetylcysteine added to standard therapy with prednisone plus azathioprine. Therapy with acetylcysteine at a dose of 600 mg three time daily, added to prednisone and azathioprine, preserves vital capacity and carbon monoxide diffusing capacity in patients with idiopathic pulmonary fibrosis better than standard therapy alone.

United States, Care and treatment, Clinical trials, Dosage and administration, Acetylcysteine, Pulmonary fibrosis

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