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Chest Hospital Heckeshorn, Berlin, Germany
Correspondence to: Mathias W. R. Pletz, MD, Department of International Health, Emory University, Atlanta, GA 30322; e-mail: mpletz{at}sph.emory.edu
To the Editor:
We read with great interest the study by Noguera et al (May 2004)1 on the apoptosis of circulating neutrophils in COPD patients. Neutrophils exhibit a short half-life and are primarily removed by apoptosis. In contrast to apoptosis, neutrophil necrosis results in the release of aggressive enzymes, leading to tissue destruction and increased inflammation.
Noguera et al compared ex vivo the spontaneous apoptosis rates of circulating neutrophils from COPD patients in stable condition with those from smokers with normal lung function and healthy nonsmokers. Since it is known that spontaneous neutrophil apoptosis is decreased in various inflammatory conditions and that neutrophils are considered to play a crucial role in COPD pathogenesis, they expected to find a decreased or delayed apoptosis. They incubated the cells and measured spontaneous apoptosis rates after 2, 8, and 24 h by flow cytometry. Surprisingly, they were not able to find a difference between the COPD patients and the control subjects. Their conclusion was that neutrophil apoptosis in COPD patients occurred at a rate similar to that found in healthy individuals and smokers with normal lung function.
We agree with the methodology used; however, we believe that this conclusion is misleading. An increase in systemic cytokines (eg, interleukin-6), inhibiting the apoptosis of circulating neutrophils,2 is present in stable-state COPD patients but is not as pronounced as in those with acute exacerbations.3 In addition, the spontaneous apoptosis rates of circulating neutrophils show a high degree of interindividual variation.4 Therefore, a larger number of subjects than that investigated by Noguera et al might be needed to find a statistically significant difference between healthy volunteers and COPD patients in the stable state.
According to the guidelines of the Global Initiative for Chronic Obstructive Lung Disease,5 exacerbations are the main factor in the progression of COPD. Therefore, we performed a very similar study but enrolled only hospitalized patients who had experienced an acute exacerbation of COPD.4 Neutrophil apoptosis was measured at hospital admission, after 3 to 5 days, and at hospital discharge. In addition, we assessed spontaneous apoptosis rates in healthy volunteers. We were able to show that neutrophil apoptosis is significantly suppressed at the beginning of an acute exacerbation (p < 0.0001 [paired t test, and the parametric distribution of the data was confirmed by the Shapiro-Wilks test]), and that it increases progressively after treatment and clinical remission, reaching the values of healthy subjects on the day of hospital discharge. Therefore, we believe that delayed neutrophil apoptosis is an important key feature of COPD pathogenesis and deserves further investigation to avoid missing any potential new treatment options for COPD, which is a disease with a high burden.
References
Hospital Universitari Son Dureta, Palma de Mallorca, Spain
Correspondence to: Aina Noguera, MD, Servei Análisi Cliniques, Hospital Universitari Son Dureta, Andrea Doria 55, Palma de Mallorca, Spain 07014; e-mail: anoguera{at}hsd.es
To the Editor:
We thank Drs. Pletz and Lode for their interest in our work (May 2004).1 We agree with their comments and suggestions. Of course, in vivo conditions may differ very substantially from in vitro ones. Thus, the comments made by Drs. Pletz and Lode with respect to our work are well taken. We would like, however, to highlight another potential source of confusion. In the article by Pletz et al,2 patients were studied during exacerbations. As such, they were receiving intense steroid therapy, among other types of therapy. As is known by the authors, steroids can interfere both with systemic inflammation3 and neutrophil apoptosis.4 We therefore fully agree with Drs. Pletz and Lode that the role of neutrophil apoptosis in COPD deserves further study.
References
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