Front. Microbiol., 10 September 2013 | doi: 10.3389/fmicb.2013.00263
- 1Department of Clinical Immunology and Internal medicine, Graduate School of Medicine, Yokohama City University, Yokohama, Japan
- 2Department of Pathology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan
Asthma is a serious health and socioeconomic issue all over the world, affecting more than 300 million individuals. The disease is considered as an inflammatory disease in the airway, leading to airway hyperresponsiveness, obstruction, mucus hyper-production and airway wall remodeling. The presence of airway inflammation in asthmatic patients has been found in the nineteenth century. As the information in patients with asthma increase, paradigm change in immunology and molecular biology have resulted in an extensive evaluation of inflammatory cells and mediators involved in the pathophysiology of asthma. Moreover, it is recognized that airway remodeling into detail, characterized by thickening of the airway wall, can be profound consequences on the mechanics of airway narrowing and contribute to the chronic progression of the disease. Epithelial to mesenchymal transition plays an important role in airway remodeling. These epithelial and mesenchymal cells cause persistence of the inflammatory infiltration and induce histological changes in the airway wall, increasing thickness of the basement membrane, collagen deposition and smooth muscle hypertrophy and hyperplasia. Resulting of airway inflammation, airway remodeling leads to the airway wall thickening and induces increased airway smooth muscle mass, which generate asthmatic symptoms. Asthma is classically recognized as the typical Th2 disease, with increased IgE levels and eosinophilic inflammation in the airway. Emerging Th2 cytokines modulates the airway inflammation, which induces airway remodeling. Biological agents, which have specific molecular targets for these Th2 cytokines, are available and clinical trials for asthma are ongoing. However, the relatively simple paradigm has been doubted because of the realization that strategies designed to suppress Th2 function are not effective enough for all patients in the clinical trials. In the future, it is required to understand more details for phenotypes of asthma.
Keywords: asthma, remodeling, epithelial to mesenchymal transition, Th2 cells, cytokines, Th17 cells, Th9 cell
Citation: Kudo M, Ishigatsubo Y and Aoki I (2013) Pathology of asthma. Front. Microbiol.4:263. doi: 10.3389/fmicb.2013.00263
Received: 30 July 2013; Accepted: 16 August 2013;
Published online: 10 September 2013.
Published online: 10 September 2013.
Edited by:
Akihide Ryo, Yokohama City University, Japan
Reviewed by:
Masatoshi Nakazawa, Yokohama City University, JapanHiroyuki Tsukagoshi, Gunma Prefectural Institute of Public Health and Environmental Sciences, Japan
Copyright © 2013 Kudo, Ishigatsubo and Aoki. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Ichiro Aoki, Department of Pathology, Graduate School of Medicine, Yokohama City University, 3-9 Fuku-ura, Kanazawa-ku Yokohama 236-0004, Japan e-mail: iaoki@med.yokohama-cu.ac.jp
No comments:
Post a Comment