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(Chest. 2000;117:285S.)
© 2000 American College of Chest Physicians

Airway Inflammation and Hyperresponsiveness to Adenosine 5'-Monophosphate in COPD*

Steven R. Rutgers, MD; Huib AM Kerstjens, MD; Wim Timens, MD; Nikolaos Tzanakis, MD; Henk F. Kauffman, PhD and Dirkje S. Postma, MD

* From the Departments of Pulmonary Diseases (Mr. Rutgers and Drs. Kerstjens and Postma), Pathology (Dr. Timens), and Allergology (Dr. Tzanakis), University Hospital Groningen, the Netherlands, and the Department of Pulmonary Disease (Dr. Kauffman), University Hospital, Crete, Greece.

Correspondence to: Steven R. Rutgers, MD, Department of Pulmonary Diseases, University Hospital Groningen, POB 30.001, 9700 RB Groningen, Netherlands


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 Introduction
 
Abbreviations: AMP = adenosine 5'-monophosphate; BHR = bronchial hyperresponsiveness

COPD is often accompanied by bronchial hyperresponsiveness (BHR). Measurement of BHR may yield information about airway inflammation, and it has been suggested that indirect stimuli might have a closer relation with inflammation than direct stimuli such as histamine or methacholine. In order to get a better understanding of the role of BHR to adenosine 5'-monophosphate (AMP) in COPD, we investigated inflammatory indices in induced sputum, BAL fluid, and bronchial biopsies. We studied 18 nonatopic, nonreversible subjects with COPD, 12 with BHR to AMP (mean ± SD age, 63 ± 8 years; FEV1 percent predicted, 56 ± 13%), and 6 without BHR to AMP (mean ± SD age, 60 ± 6 years; FEV1 percent predicted, 65 ± 11%), and compared these with 11 healthy nonatopic control subjects (mean ± SD age, 58 ± 8 years; FEV1 percent predicted, 104 ± 11%).

Subjects with COPD with BHR in comparison to those without BHR had significantly higher numbers of mucosal CD8+ cells (median, 550 cells/µL; range, 30 to 1,340 cells/mm2 vs median, 280 cells/µL; range, 110 to 450 cells/mm2, p = 0.045) and higher percentages of sputum eosinophils (median, 2.7%; range, 0.5 to 8.5% vs median, 0.6%; range, 0 to 0.8%, p = 0.004). Otherwise, no differences between the two groups with COPD were observed.

We submit that hyperresponsiveness to AMP in COPD is associated with airway inflammation that is characterized by increased numbers of mucosal CD8+ cells and sputum eosinophils. A logical next step is to investigate whether AMP is a marker of inflammation in COPD that has prognostic relevance for the course of the disease and for the effects of treatments, including steroids.





This Article
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Right arrow Articles by Rutgers, S. R.
Right arrow Articles by Postma, D. S.


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