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Mediators of Inflammation
Volume 2013 (2013), Article ID 413735, 9 pages
Review Article

Inflammation and Immune Response in COPD: Where Do We Stand?

Intensive Care Unit, 1st Department of Respiratory Medicine, Medical School, National and Kapodistrian University of Athens and “Sotiria” Chest Disease Hospital, 152 Mesogeion Avenue, 11527 Athens, Greece

Received 12 February 2013; Accepted 2 July 2013

Academic Editor: Helen C. Steel

Copyright © 2013 Nikoletta Rovina et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Increasing evidence indicates that chronic inflammatory and immune responses play key roles in the development and progression of COPD. Recent data provide evidence for a role in the NLRP3 inflammasome in the airway inflammation observed in COPD. Cigarette smoke activates innate immune cells by triggering pattern recognition receptors (PRRs) to release “danger signal”. These signals act as ligands to Toll-like receptors (TLRs), triggering the production of cytokines and inducing innate inflammation. In smokers who develop COPD there appears to be a specific pattern of inflammation in the airways and parenchyma as a result of both innate and adaptive immune responses, with the predominance of CD8+ and CD4+ cells, and in the more severe disease, with the presence of lymphoid follicles containing B lymphocytes and T cells. Furthermore, viral and bacterial infections interfere with the chronic inflammation seen in stable COPD and exacerbations via pathogen-associated molecular patterns (PAMPs). Finally, autoimmunity is another novel aspect that may play a critical role in the pathogenesis of COPD. This review is un update of the currently discussed roles of inflammatory and immune responses in the pathogenesis of COPD.