Chest ACCP Education Calendar
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cosio, M. G.
Right arrow Articles by Cosio, M. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cosio, M. G.
Right arrow Articles by Cosio, M. G.
(Chest. 2002;121:160S-165S.)
© 2002 American College of Chest Physicians

Inflammation of the Airways and Lung Parenchyma in COPD*

Role of T Cells

Manuel G. Cosio, MD; Joaquim Majo, MD and Monica G. Cosio, MD

* From the McGill University (Dr. Manuel Cosio), Royal Victoria Hospital, Montreal, PQ, Canada; the Department d’Anatomia Patologica (Dr. Majo), Hospitals Universitaris Vall d’Hebron, Barcelona, Spain; and the Department of Pathology (Dr. Monica Cosio), Ramon y Cajal University Hospital, Madrid, Spain.

Correspondence to: Manuel G. Cosio, MD, Professor of Medicine, McGill University, Royal Victoria Hospital, Respiratory Division, Room L4.11, 687 Pine Ave West, Montreal, PQ H3A 1A1 Canada; e-mail: manuel.cosio{at}muhc.mcgill.ca

A smoking-induced inflammatory reaction in the airways and lung parenchyma, comprised mainly of neutrophils and alveolar macrophages, has long been accepted to be the major cause of COPD in smokers. Recent reports have underlined the role of the T lymphocyte as a potentially important factor in the inflammatory process leading to COPD. It has been found that, in the airways and the lung parenchyma, the presence of T cells, predominantly CD8+ T cells, can distinguish between smokers with and without COPD. In addition to T cells, other inflammatory cell types such as neutrophils and macrophages are probably essential in the initial inflammatory process leading to the breakdown of lung tissue, perhaps producing peptides eventually recognized by T cells as antigenic. This would provide an explanation for the T-cell inflammation. Once activated, T cells are present in the lung, and their effector functions would include the attraction and enhancement of the inflammatory function in other inflammatory cells like neutrophils and macrophages. It seems likely that, only when all inflammatory cell types (ie, CD4+, CD8+, neutrophils, and macrophages) are present in the lung, the airways remodeling and parenchymal destruction characteristic of COPD will ensue. If T cells are responsible for the lung injury and progression of COPD, it would resemble a response to an antigenic stimulus originating in the lung. If that were the case, COPD could be considered to be an autoimmune disease triggered by smoking.

Key Words: airways inflammation • antigen presentation • apoptosis • auto-immunity • cigarette smoke • COPD • emphysema • T cell




This article has been cited by other articles:


Home page
 ChestHome page
C. Costa, R. Rufino, S. L. Traves, J. R. Lapa e Silva, P. J. Barnes, and L. E. Donnelly
CXCR3 and CCR5 Chemokines in Induced Sputum From Patients With COPD
Chest, January 1, 2008; 133(1): 26 - 33.
[Abstract] [Full Text] [PDF]

Home page
 ChestHome page
S. Baraldo, E. Bazzan, M. E. Zanin, G. Turato, S. Garbisa, P. Maestrelli, A. Papi, M. Miniati, L. M. Fabbri, R. Zuin, et al.
Matrix Metalloproteinase-2 Protein in Lung Periphery Is Related to COPD Progression
Chest, December 1, 2007; 132(6): 1733 - 1740.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
K. R. Bracke, A. I. D'hulst, T. Maes, K. B. Moerloose, I. K. Demedts, S. Lebecque, G. F. Joos, and G. G. Brusselle
Cigarette Smoke-Induced Pulmonary Inflammation and Emphysema Are Attenuated in CCR6-Deficient Mice
J. Immunol., October 1, 2006; 177(7): 4350 - 4359.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
S. Escotte, D. Al Alam, R. Le Naour, E. Puchelle, M. Guenounou, and S. C. Gangloff
T Cell Chemotaxis and Chemokine Release after Staphylococcus aureus Interaction with Polarized Airway Epithelium
Am. J. Respir. Cell Mol. Biol., March 1, 2006; 34(3): 348 - 354.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
A. K. Sullivan, P. L. Simonian, M. T. Falta, J. D. Mitchell, G. P. Cosgrove, K. K. Brown, B. L. Kotzin, N. F. Voelkel, and A. P. Fontenot
Oligoclonal CD4+ T Cells in the Lungs of Patients with Severe Emphysema
Am. J. Respir. Crit. Care Med., September 1, 2005; 172(5): 590 - 596.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
L. Taraseviciene-Stewart, R. Scerbavicius, K.-H. Choe, M. Moore, A. Sullivan, M. R. Nicolls, A. P. Fontenot, R. M. Tuder, and N. F. Voelkel
An Animal Model of Autoimmune Emphysema
Am. J. Respir. Crit. Care Med., April 1, 2005; 171(7): 734 - 742.
[Abstract] [Full Text] [PDF]

Home page
 Pharmacol. Rev.Home page
P. J. Barnes
Mediators of Chronic Obstructive Pulmonary Disease
Pharmacol. Rev., December 1, 2004; 56(4): 515 - 548.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
D. Bruder, A. M. Westendorf, R. Geffers, A. D. Gruber, M. Gereke, R. I. Enelow, and J. Buer
CD4 T Lymphocyte-mediated Lung Disease: Steady State between Pathological and Tolerogenic Immune Reactions
Am. J. Respir. Crit. Care Med., December 1, 2004; 170(11): 1145 - 1152.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
A. Guerassimov, Y. Hoshino, Y. Takubo, A. Turcotte, M. Yamamoto, H. Ghezzo, A. Triantafillopoulos, K. Whittaker, J. R. Hoidal, and M. G. Cosio
The Development of Emphysema in Cigarette Smoke-exposed Mice Is Strain Dependent
Am. J. Respir. Crit. Care Med., November 1, 2004; 170(9): 974 - 980.
[Abstract] [Full Text] [PDF]

Home page
 Eur Respir JHome page
M.G. Cosio
Autoimmunity, T-cells and STAT-4 in the pathogenesis of chronic obstructive pulmonary disease
Eur. Respir. J., July 1, 2004; 24(1): 3 - 5.
[Full Text] [PDF]

Home page
 Eur Respir JHome page
A. Di Stefano, G. Caramori, A. Capelli, I. Gnemmi, F.L. Ricciardolo, T. Oates, C.F. Donner, K.F. Chung, P.J. Barnes, and I.M. Adcock
STAT4 activation in smokers and patients with chronic obstructive pulmonary disease
Eur. Respir. J., July 1, 2004; 24(1): 78 - 85.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
D. Massaro, G. D. Massaro, A. Baras, E. P. Hoffman, and L. B. Clerch
Calorie-related rapid onset of alveolar loss, regeneration, and changes in mouse lung gene expression
Am J Physiol Lung Cell Mol Physiol, May 1, 2004; 286(5): L896 - L906.
[Abstract] [Full Text] [PDF]

Home page
 Eur Respir JHome page
P.J. Barnes, S.D. Shapiro, and R.A. Pauwels
Chronic obstructive pulmonary disease: molecular and cellularmechanisms
Eur. Respir. J., October 1, 2003; 22(4): 672 - 688.
[Abstract] [Full Text] [PDF]

Home page
 Occup. Environ. Med.Home page
E Hnizdo and V Vallyathan
Chronic obstructive pulmonary disease due to occupational exposure to silica dust: a review of epidemiological and pathological evidence
Occup. Environ. Med., April 1, 2003; 60(4): 237 - 243.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2002 by the American College of Chest Physicians.