Thorax 2001;56:36-41 ( January )

Relationship between airway inflammation and the frequency of exacerbations in patients with smoking related COPD

S Gompertz, D L Bayley, S L Hill, R A Stockley

Department of Respiratory Medicine, Queen Elizabeth Hospital, Birmingham B15 2TH, UK

Correspondence to: Dr S Gompertz, Lung Investigation Unit, Queen Elizabeth Hospital, Birmingham B15 2TH, UK sgompertz{at}doctors.net

Received 15 June 2000; Returned to authors 22 August 2000; Revised version received 11 September 2000; Accepted for publication 25 September 2000

BACKGROUNDPatients with more frequent exacerbations of chronic obstructive pulmonary disease (COPD) may have increased bronchial inflammation. Airway inflammation was measured in patients who had been thoroughly investigated with full pulmonary function testing, thoracic HRCT scanning, and sputum microbiology to examine further the relationship between exacerbation frequency and bronchial inflammation.
METHODSAirway inflammation (spontaneous sputum sol phase myeloperoxidase (MPO), elastase, leukotriene (LT)B₄, interleukin (IL)-8, secretory leukoprotenase inhibitor (SLPI), protein leakage) and serum levels of C reactive protein (CRP) were compared in 40 patients with stable, smoking related COPD, divided into those with frequent (3/year) or infrequent (2/year) exacerbations according to the number of primary care consultations during the preceding year. The comparisons were repeated after excluding eight otherwise clinically indistinguishable patients who had tubular bronchiectasis on the HRCT scan.
RESULTSPatients with frequent (n=12) and infrequent (n=28) exacerbations were indistinguishable in terms of their clinical, pulmonary function, and sputum characteristics, CRP concentrations, and all of their bronchial inflammatory parameters (p>0.05). The patients without evidence of tubular bronchiectasis (n=32) were equally well matched but the sputum concentrations of SLPI were significantly lower in the frequent exacerbators (n=8) in this subset analysis (p<0.05).
CONCLUSIONSThere are several clinical features that directly influence bronchial inflammation in COPD. When these were carefully controlled for, patients with more frequent reported exacerbations had lower sputum concentrations of SLPI. This important antiproteinase is also known to possess antibacterial and antiviral activity. Further studies are required into the nature of recurrent exacerbations and, in particular, the regulation and role of SLPI in affected individuals.


Keywords: chronic obstructive pulmonary disease; inflammation; secretory leukoprotease inhibitor (SLPI)

---

© 2001 by Thorax
CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

• Tamagawa, E., Suda, K., Yuan Wei, , Li Xing, , Mui, T., Yuexin Li, , van Eeden, S. F., Man, S.F. P., Sin, D. D. (2009). Endotoxin-induced translocation of interleukin-6 from lungs to the systemic circulation. Innate Immunity 15: 251-258 [Abstract]  
• de Oca, M. M., Talamo, C., Halbert, R. J., Perez-Padilla, R., Lopez, M. V., Muino, A., Jardim, J. R. B., Valdivia, G., Pertuze, J., Moreno, D., Menezes, A. M. B. (2009). Frequency of Self-Reported COPD Exacerbation and Airflow Obstruction in Five Latin American Cities: The Proyecto Latinoamericano de Investigacion en Obstruccion Pulmonar (PLATINO) Study. Chest 136: 71-78 [Abstract] [Full Text]  
• Anzueto, A., Miravitlles, M. (2009). Efficacy of tiotropium in the prevention of exacerbations of COPD. Ther Adv Respir Dis 3: 103-111 [Abstract]  
• Rahman, I. (2008). Review: Antioxidant therapeutic advances in COPD. Ther Adv Respir Dis 2: 351-374 [Abstract]  
• Sethi, S., Murphy, T. F. (2008). Infection in the Pathogenesis and Course of Chronic Obstructive Pulmonary Disease. NEJM 359: 2355-2365 [Full Text]  
• Sapey, E, Bayley, D, Ahmad, A, Newbold, P, Snell, N, Stockley, R A (2008). Inter-relationships between inflammatory markers in patients with stable COPD with bronchitis: intra-patient and inter-patient variability. Thorax 63: 493-499 [Abstract] [Full Text]  
• Cazzola, M., MacNee, W., Martinez, F. J., Rabe, K. F., Franciosi, L. G., Barnes, P. J., Brusasco, V., Burge, P. S., Calverley, P. M. A., Celli, B. R., Jones, P. W., Mahler, D. A., Make, B., Miravitlles, M., Page, C. P., Palange, P., Parr, D., Pistolesi, M., Rennard, S. I., Rutten-van Molken, M. P., Stockley, R., Sullivan, S. D., Wedzicha, J. A., Wouters, E. F., on behalf of the American Thoracic Society/Europea, (2008). Outcomes for COPD pharmacological trials: from lung function to biomarkers. Eur Respir J 31: 416-469 [Abstract] [Full Text]  
• Anzueto, A., Sethi, S., Martinez, F. J. (2007). Exacerbations of Chronic Obstructive Pulmonary Disease. Proc Am Thorac Soc 4: 554-564 [Abstract] [Full Text]  
• Rahman, I., Adcock, I. M. (2006). Oxidative stress and redox regulation of lung inflammation in COPD.. Eur Respir J 28: 219-242 [Abstract] [Full Text]  
• Fernaays, M. M., Lesse, A. J., Sethi, S., Cai, X., Murphy, T. F. (2006). Differential Genome Contents of Nontypeable Haemophilus influenzae Strains from Adults with Chronic Obstructive Pulmonary Disease.. Infect. Immun. 74: 3366-3374 [Abstract] [Full Text]  
• Roghanian, A., Williams, S. E., Sheldrake, T. A., Brown, T. I., Oberheim, K., Xing, Z., Howie, S. E. M., Sallenave, J.-M. (2006). The Antimicrobial/Elastase Inhibitor Elafin Regulates Lung Dendritic Cells and Adaptive Immunity. Am. J. Respir. Cell Mol. Bio. 34: 634-642 [Abstract] [Full Text]  
• Sapey, E, Stockley, R A (2006). COPD exacerbations {middle dot} 2: Aetiology.. Thorax 61: 250-258 [Abstract] [Full Text]  
• Tsoumakidou, M., Tzanakis, N., Chrysofakis, G., Siafakas, N. M. (2005). Nitrosative Stress, Heme Oxygenase-1 Expression and Airway Inflammation During Severe Exacerbations of COPD. Chest 127: 1911-1918 [Abstract] [Full Text]  
• Kim, S., Emerman, C. L., Cydulka, R. K., Rowe, B. H., Clark, S., Camargo, C. A. (2004). Prospective Multicenter Study of Relapse Following Emergency Department Treatment of COPD Exacerbation. Chest 125: 473-481 [Abstract] [Full Text]  
• Barnes, P.J., Shapiro, S.D., Pauwels, R.A. (2003). Chronic obstructive pulmonary disease: molecular and cellularmechanisms. Eur Respir J 22: 672-688 [Abstract] [Full Text]  
• White, A J, Gompertz, S, Bayley, D L, Hill, S L, O'Brien, C, Unsal, I, Stockley, R A (2003). Resolution of bronchial inflammation is related to bacterial eradication following treatment of exacerbations of chronic bronchitis. Thorax 58: 680-685 [Abstract] [Full Text]  
• Biernacki, W A, Kharitonov, S A, Barnes, P J (2003). Increased leukotriene B4 and 8-isoprostane in exhaled breath condensate of patients with exacerbations of COPD. Thorax 58: 294-298 [Abstract] [Full Text]  
• White, A J, Gompertz, S, Stockley, R A (2003). Chronic obstructive pulmonary disease * 6: The aetiology of exacerbations of chronic obstructive pulmonary disease. Thorax 58: 73-80 [Abstract] [Full Text]  
• Miravitlles, M. (2002). Exacerbations of chronic obstructive pulmonary disease: when are bacteria important?. Eur Respir J 20: 9S-19s [Abstract] [Full Text]  
• Kelly, M, Dentener, M A, Creutzberg, E C, Wouters, E F M (2002). Pathophysiology of COPD. Thorax 57: 563-564 [Full Text]