HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:
Guest Access | Sign In via User Name/Password

This Article Full Text Free Full Text (PDF) Free Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Article Archive Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (10) Citing Articles via Google Scholar Google Scholar Articles by Jeffery, P. K. Search for Related Content PubMed PubMed Citation Articles by Jeffery, P. K.

Comparison of the Structural and Inflammatory Features of COPD and Asthma^* Giles F. Filley Lecture

^* From the Imperial College School of Medicine at the Royal Brompton Hospital, London, UK.

Correspondence to: Peter K. Jeffery, DSc (Med), Lung Pathology Unit, Royal Brompton Hospital, Sydney St, London, SW3 6NP, UK; e-mail: p.jeffery{at}ic.ac.uk

At least three conditions contribute to COPD. (1) Chronic bronchitis (mucous hypersecretion) is an inflammatory condition in which CD8+ T-lymphocytes, neutrophils, and CD68+ monocytes/macrophages predominate. The condition is defined clinically by the presence of chronic cough and recurrent increases in bronchial secretions sufficient to cause expectoration. There is enlargement of mucus-secreting glands and goblet cell hyperplasia, which can occur in the absence of airflow limitation. (2) Adult chronic bronchiolitis (small or peripheral airways disease) is an inflammatory condition of small bronchi and bronchioli in which there are predominantly CD8+ and pigmented macrophages. The functional defect is difficult to detect clinically but may be recognized by sophisticated tests of small airway function. There is mucous metaplasia, enlargement of the mass of bronchiolar smooth muscle, and loss of alveolar attachments. (3) Emphysema is an inflammatory condition of the alveoli in which T-lymphocytes, neutrophils, and pigmented alveolar macrophages are involved, associated with the release of excessive amounts of elastases. It is defined anatomically by permanent, destructive enlargement of airspaces distal to terminal bronchioli without obvious fibrosis. In contrast, asthma is a clinical syndrome characterized by allergic inflammation of bronchi and bronchioli in which CD4+ (helper) T-lymphocytes and eosinophils predominate. There is increased production and release of interleukin (IL)-4 and IL-5, which is referred to as a Th2-type response. There is usually increased tracheobronchial responsiveness to a variety of stimuli, and the condition is usually manifest as variable airflow obstruction. While differences between COPD and asthma have been highlighted, new data are emerging that indicate there may also be similarities.

Key Words: airway • asthma • biopsy • chronic bronchitis • COPD • emphysema • inflammation

This article has been cited by other articles:

				F. Guddo, A. M. Vignola, M. Saetta, S. Baraldo, L. Siena, E. Balestro, R. Zuin, A. Papi, P. Maestrelli, L. M. Fabbri, et al. Upregulation of basic fibroblast growth factor in smokers with chronic bronchitis Eur. Respir. J., May 1, 2006; 27(5): 957 - 963. [Abstract] [Full Text] [PDF]

				P. W. Jones and A. G. N. Agusti Outcomes and markers in the assessment of chronic obstructive pulmonary disease. Eur. Respir. J., April 1, 2006; 27(4): 822 - 832. [Abstract] [Full Text] [PDF]

				L. K. A. Lundblad, J. Thompson-Figueroa, T. Leclair, M. J. Sullivan, M. E. Poynter, C. G. Irvin, and J. H. T. Bates Tumor Necrosis Factor-{alpha} Overexpression in Lung Disease: A Single Cause behind a Complex Phenotype Am. J. Respir. Crit. Care Med., June 15, 2005; 171(12): 1363 - 1370. [Abstract] [Full Text] [PDF]

				R. Gosens, I. S. T. Bos, J. Zaagsma, and H. Meurs Protective Effects of Tiotropium Bromide in the Progression of Airway Smooth Muscle Remodeling Am. J. Respir. Crit. Care Med., May 15, 2005; 171(10): 1096 - 1102. [Abstract] [Full Text] [PDF]

				U. Lappalainen, J. A. Whitsett, S. E. Wert, J. W. Tichelaar, and K. Bry Interleukin-1{beta} Causes Pulmonary Inflammation, Emphysema, and Airway Remodeling in the Adult Murine Lung Am. J. Respir. Cell Mol. Biol., April 1, 2005; 32(4): 311 - 318. [Abstract] [Full Text] [PDF]

				M. Laan, S. Bozinovski, and G. P. Anderson Cigarette Smoke Inhibits Lipopolysaccharide-Induced Production of Inflammatory Cytokines by Suppressing the Activation of Activator Protein-1 in Bronchial Epithelial Cells J. Immunol., September 15, 2004; 173(6): 4164 - 4170. [Abstract] [Full Text] [PDF]

				S V Culpitt, D F Rogers, P S Fenwick, P Shah, C De Matos, R E K Russell, P J Barnes, and L E Donnelly Inhibition by red wine extract, resveratrol, of cytokine release by alveolar macrophages in COPD Thorax, November 1, 2003; 58(11): 942 - 946. [Abstract] [Full Text] [PDF]

				Y. Chen, P. Thai, Y.-H. Zhao, Y.-S. Ho, M. M. DeSouza, and R. Wu Stimulation of Airway Mucin Gene Expression by Interleukin (IL)-17 through IL-6 Paracrine/Autocrine Loop J. Biol. Chem., May 2, 2003; 278(19): 17036 - 17043. [Abstract] [Full Text] [PDF]

				H. J. Patel, M. G. Belvisi, D. Bishop-Bailey, M. H. Yacoub, and J. A. Mitchell Activation of Peroxisome Proliferator-Activated Receptors in Human Airway Smooth Muscle Cells Has a Superior Anti-inflammatory Profile to Corticosteroids: Relevance for Chronic Obstructive Pulmonary Disease Therapy J. Immunol., March 1, 2003; 170(5): 2663 - 2669. [Abstract] [Full Text] [PDF]

				D.D. Sin and S.F.P. Man Inhaled corticosteroids and survival in chronic obstructive pulmonary disease: does the dose matter? Eur. Respir. J., February 1, 2003; 21(2): 260 - 266. [Abstract] [Full Text] [PDF]

				L. M. Fabbri, M. Romagnoli, L. Corbetta, G. Casoni, K. Busljetic, G. Turato, G. Ligabue, A. Ciaccia, M. Saetta, and A. Papi Differences in Airway Inflammation in Patients with Fixed Airflow Obstruction Due to Asthma or Chronic Obstructive Pulmonary Disease Am. J. Respir. Crit. Care Med., February 1, 2003; 167(3): 418 - 424. [Abstract] [Full Text] [PDF]

				S. V. Culpitt, D. F. Rogers, P. Shah, C. De Matos, R. E. K. Russell, L. E. Donnelly, and P. J. Barnes Impaired Inhibition by Dexamethasone of Cytokine Release by Alveolar Macrophages from Patients with Chronic Obstructive Pulmonary Disease Am. J. Respir. Crit. Care Med., January 1, 2003; 167(1): 24 - 31. [Abstract] [Full Text] [PDF]

				M. Saetta and G. Turato Airway pathology in asthma Eur. Respir. J., July 2, 2001; 18(34_suppl): 18S - 23s. [Abstract] [Full Text] [PDF]

				Z. Wang, T. Zheng, Z. Zhu, R. J. Homer, R. J. Riese, H. A. Chapman , Jr., S. D. Shapiro, and J. A. Elias Interferon {{gamma}} Induction of Pulmonary Emphysema in the Adult Murine Lung J. Exp. Med., December 4, 2000; 192(11): 1587 - 1600. [Abstract] [Full Text] [PDF]