Abstract
Asthma and chronic obstructive pulmonary disease (COPD) are two different inflammatory disorders of the lungs which share a common functional abnormality, i.e. airflow limitation [1,2]. In asthma, airflow limitation is largely reversible, either spontaneously or with treatment, and does not progress in most cases [1]. On the other hand, airflow limitation in COPD is usually progressive and poorly reversible [2]. In asthma, the chronic inflammation causes an associated increase in airway responsiveness to a variety of stimuli, leading to recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night and in the early morning. Many cells are involved in the inflammatory response in asthma and, among these, CD4+ Type-2 lymphocytes, mast cells and eosinophils are thought to play a crucial role. In COPD, the poorly reversible airflow limitation is associated with an abnormal inflammatory response of the lungs to noxious particles or gases [2]. This chronic inflammation is characterized by an increased number of CD8+ Type-1 T-lymphocytes and macrophages in the lung tissue and neutrophils in the airway lumen. Lymphocytes, which are markedly different in the two inflammatory conditions, play a crucial role in the pathogenesis of asthma and COPD. In this review, we will discuss the current concepts on the recruitment, homing and activity of lymphocytes in these two respiratory diseases.
Keywords: Pulmonary inflammation, airflow limitation, cytokines, chemokines
Current Medicinal Chemistry
Title: The Role of Lymphocytes in the Pathogenesis of Asthma and COPD
Volume: 14 Issue: 21
Author(s): Simonetta Baraldo, Kim Lokar Oliani, Graziella Turato, Renzo Zuin and Marina Saetta
Affiliation:
Keywords: Pulmonary inflammation, airflow limitation, cytokines, chemokines
Abstract: Asthma and chronic obstructive pulmonary disease (COPD) are two different inflammatory disorders of the lungs which share a common functional abnormality, i.e. airflow limitation [1,2]. In asthma, airflow limitation is largely reversible, either spontaneously or with treatment, and does not progress in most cases [1]. On the other hand, airflow limitation in COPD is usually progressive and poorly reversible [2]. In asthma, the chronic inflammation causes an associated increase in airway responsiveness to a variety of stimuli, leading to recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night and in the early morning. Many cells are involved in the inflammatory response in asthma and, among these, CD4+ Type-2 lymphocytes, mast cells and eosinophils are thought to play a crucial role. In COPD, the poorly reversible airflow limitation is associated with an abnormal inflammatory response of the lungs to noxious particles or gases [2]. This chronic inflammation is characterized by an increased number of CD8+ Type-1 T-lymphocytes and macrophages in the lung tissue and neutrophils in the airway lumen. Lymphocytes, which are markedly different in the two inflammatory conditions, play a crucial role in the pathogenesis of asthma and COPD. In this review, we will discuss the current concepts on the recruitment, homing and activity of lymphocytes in these two respiratory diseases.
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Cite this article as:
Baraldo Simonetta, Oliani Kim Lokar, Turato Graziella, Zuin Renzo and Saetta Marina, The Role of Lymphocytes in the Pathogenesis of Asthma and COPD, Current Medicinal Chemistry 2007; 14 (21) . https://dx.doi.org/10.2174/092986707781696573
DOI https://dx.doi.org/10.2174/092986707781696573 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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