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We know that neutrophils can lead to chronic lung diseases not so much by acting to defend us against bacterial and viral infections, but by promoting the inflammatory response. Chronic obstructive pulmonary disease (COPD), asthma, cystic fibrosis, and acute respiratory distress syndrome all develop through mechanisms related to a prolonged inflammatory response.


Recent research supports that the activity of a neutrophil enzyme, leukotriene A4 hydrolase, may provide a therapeutic approach for treating chronic lung disease. Cigarette smoking leads to COPD through the chronic inflammation and tissue damage mediated by prolonged neutrophilic activity. Snelgrove et al determined that cigarette smoke reduced activity of the enzyme leukotriene A4 hydrolase. Normally, this enzyme inactivates a chemical attractant for neutrophils, pro-gly-pro. However, in the absence of leukotriene A4 hydrolase, the pro-gly-pro remained active in the lungs of cigarette smokers and increased neutrophil migration into lung tissues. The prolonged neutrophil activity contributes to increased inflammation, lung damage, and respiratory dysfunction.


Identifying this mechanism that contributes to lung damage caused by cigarette smoking is encouraging. Pharmaceutical research can focus on developing drugs that block the abnormal activity of pro-gly-pro in smokers. This strategy might be useful in treating neturophilic inflammation and decrease development of inflammatory-mediated COPD. However, nurses know that without a doubt not smoking is the best strategy to reduce lung damage.


Source: Barnes P. Neutrophils find smoke attractive. Science. 2010;330(6000):40-41. Available at Accessed October 31, 2010.


Submitted by: Robin E. Pattillo, PhD, RN, CNL, News Editor at