Abstract
COPD (Chronic Obstructive Pulmonary Disease) is an important lung and airway disease which affects the lives of around 200 million people worldwide with an increasing incidence particularly in developing countries. The pathogenesis of COPD is based on the innate and adaptive inflammatory immune response to the inhalation of toxic particles and gases. Although cigarette smoking is the primary cause of this inflammation, many other environmental and occupational exposures contribute to the pathology of COPD. The immune inflammatory changes associated with COPD are linked to a tissue repair and remodeling process that increases mucus production and causes emphysematous destruction of the gas-exchanging surface of the lung. The inflamed airways of COPD patients contain several inflammatory cells including neutrophils, macrophages, T lymphocytes, and dendritic cells (DCs). Little is known about the relative contribution of DCs in the pathogenesis of COPD. However the number of DCs is changed in smokers and COPD patients and cigarette smoke (CS) induces the release of chemokines from DCs that play a role in the pathogenesis of COPD.
In this review paper, an overview is presented on the role of DCs and their mediators in the pathogenesis of COPD. The activation of DCs and their signaling in response to CS will also be highlighted and discussed.
Keywords: DCs, COPD, emphysema, inflammation
Current Pharmaceutical Design
Title:Dendritic Cells in Pathogenesis of COPD
Volume: 18 Issue: 16
Author(s): Masoumeh Ezzati Givi, Frank A. Redegeld, Gert Folkerts and Esmaeil Mortaz
Affiliation:
Keywords: DCs, COPD, emphysema, inflammation
Abstract: COPD (Chronic Obstructive Pulmonary Disease) is an important lung and airway disease which affects the lives of around 200 million people worldwide with an increasing incidence particularly in developing countries. The pathogenesis of COPD is based on the innate and adaptive inflammatory immune response to the inhalation of toxic particles and gases. Although cigarette smoking is the primary cause of this inflammation, many other environmental and occupational exposures contribute to the pathology of COPD. The immune inflammatory changes associated with COPD are linked to a tissue repair and remodeling process that increases mucus production and causes emphysematous destruction of the gas-exchanging surface of the lung. The inflamed airways of COPD patients contain several inflammatory cells including neutrophils, macrophages, T lymphocytes, and dendritic cells (DCs). Little is known about the relative contribution of DCs in the pathogenesis of COPD. However the number of DCs is changed in smokers and COPD patients and cigarette smoke (CS) induces the release of chemokines from DCs that play a role in the pathogenesis of COPD.
In this review paper, an overview is presented on the role of DCs and their mediators in the pathogenesis of COPD. The activation of DCs and their signaling in response to CS will also be highlighted and discussed.
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Cite this article as:
Ezzati Givi Masoumeh, A. Redegeld Frank, Folkerts Gert and Mortaz Esmaeil, Dendritic Cells in Pathogenesis of COPD, Current Pharmaceutical Design 2012; 18 (16) . https://dx.doi.org/10.2174/138161212800166068
DOI https://dx.doi.org/10.2174/138161212800166068 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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