Molecular Mechanisms of Metaplasia, Differentiation and Hyperplasia of Goblet Cellin Allergic AsthmaToshiharu Hayashi*
Department of Veterinary Medicine, Yamaguchi University, Japan
- *Corresponding Author:
- Toshiharu Hayashi
Laboratory of Veterinary Pathology
Joint Faculty of Veterinary Medicine
Yamaguchi University, 1677-1
Tel/Fax: +81 83 933 5890
E-mail: [email protected]
Received date: August 01, 2012; Accepted date: October 25, 2012; Published date: November 30, 2012
Citation: Hayashi T (2012) Molecular Mechanisms of Metaplasia, Differentiation and Hyperplasia of Goblet Cellin Allergic Asthma. J Aller Ther 3:121. doi: 10.4172/2155-6121.1000121
Copyright: © 2012 Hayashi T. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Bronchial allergic asthma (asthma) is an airway inflammation characterized by airflow obstruction of variable degrees with bronchial hyper-responsiveness and is induced by a complex interaction of environmental and genetic factors. Asthma of the human can be divided into an immediate- and a late-phase reaction, and some of the patients develop a late-phase reaction after a symptom-free interval. Hallmarks of asthma are mucus overproduction by goblet cells associated with responses of helper T(Th)2 cells. Mucus hypersecretion from goblet cells themselves or by metaplasia and/or hyperplasia of goblet cells appears to be associated with disease severity in asthma, because mucus production by those cells in local bronchial–bronchiolar lesions causes airway mucus plugging. However, the mechanisms of mucus production are not fully understood. Molecular mechanisms of goblet cell metaplasia, differentiation and hyperplasia will be reviewed in this article. Also, the relationship between allergic inflammation in Th1/Th2 paradigm shift and thymic stromal lymphopoietin (TSLP) was included for the understanding of goblet cell response in asthma. The clarification of mechanisms of mucin production in vivo may lead to the development of novel therapeutic strategies to suppress mucus production in asthma.