Airway inflammation and hyperresponsiveness to adenosine 5 '-monophosphatein chronic obstructive pulmonary disease

Citation
Sr. Rutgers et al., Airway inflammation and hyperresponsiveness to adenosine 5 '-monophosphatein chronic obstructive pulmonary disease, CLIN EXP AL, 30(5), 2000, pp. 657-662
Citations number
28
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
CLINICAL AND EXPERIMENTAL ALLERGY
ISSN journal
09547894 → ACNP
Volume
30
Issue
5
Year of publication
2000
Pages
657 - 662
Database
ISI
SICI code
0954-7894(200005)30:5<657:AIAHTA>2.0.ZU;2-E
Abstract
Background Chronic obstructive pulmonary disease (COPD) is often accompanie d by bronchial hyperresponsiveness (BHR). Measurement of BHR may give infor mation about airway inflammation. Objective To investigate the role of airway inflammation in hyperresponsive ness to adenosine 5'-monophosphate (AMP) in COPD. Methods We investigated inflammatory indices in induced sputum, bronchoalve olar lavage (BAL) fluid and bronchial biopsies in subjects with COPD with a nd without hyperresponsiveness to AMP. Twelve nonatopic subjects with COPD with hyperresponsiveness to AMP (mean +/- SD, age 63 +/- 8 years, FEV1% pre dicted 56 +/- 13%), six without BHR (age 60 +/- 6 years, FEV1% predicted 65 +/- 11%) and 11 healthy nonatopic controls without BHR (age 58 +/- 8 years , FEV1% predicted 104 +/- 11%) participated in the study. Results Subjects with COPD with BHR had significantly higher numbers of muc osal CD8 + and higher percentages of sputum eosinophils than those without BHR (median, 550 cells/mm(2); range, 30-1340 vs 280 cells/mm(2); range, 110 -450, P = 0.045; and median, 2.7%; range, 0.5-8.5 vs 0.6%; range, 0-0.8 %, P = 0.0036, respectively). No differences were observed in BAL fluid. Conclusion We conclude that hyperresponsiveness to AMP in COPD is associate d with airway inflammation that is characterized by increased numbers of mu cosal CD8 + cells and percentages of sputum eosinophils. Hyperresponsivenes s to AMP may be used as a marker of airway inflammation in COPD, but its si gnificance in the clinical course remains to be determined.