Abstract
Mucus production is a cardinal feature of bronchial asthma, contributing to morbidity and mortality in the disease. Goblet cells are major mucus-producing cells, and goblet cell hyperplasia (GCH) is one feature of airway remodeling, defined as structural changes occurring in the airway. A number of studies have demonstrated that Th2-type cells play critical roles in this process and that particularly interleukin-13 (IL-13), among Th2-type cytokines, is a central mediator for GCH. However, the mechanism underlying how Th2 cytokines induce mucus production or GCH is poorly understood. Mouse calcium-activated chloride channel-3 (mCLCA-3; gob-5)/human CLCA-1 acts as a downstream molecule of Th2 cytokines, IL-4/IL-9/IL-13 signals, playing an important role in mucus production. Moreover, we have recently found that pendrin, an anion transporter, is induced by IL-13 and causes mucus production in airway epithelial cells. It is hoped that if we can clarify how mucus is produced, this will lead to development of novel therapeutic reagents to suppress mucus production in bronchial asthma.
Keywords: Mucus, bronchial asthma, goblet cell hyperplasia, MUC5AC, Th2 cytokine, pendrin, calciumactivated chloride channel
Current Medicinal Chemistry
Title: The Mechanism of Mucus Production in Bronchial Asthma
Volume: 16 Issue: 22
Author(s): K. Izuhara, S. Ohta, H. Shiraishi, S. Suzuki, K. Taniguchi, S. Toda, T. Tanabe, M. Yasuo, K. Kubo, T. Hoshino and H. Aizawa
Affiliation:
Keywords: Mucus, bronchial asthma, goblet cell hyperplasia, MUC5AC, Th2 cytokine, pendrin, calciumactivated chloride channel
Abstract: Mucus production is a cardinal feature of bronchial asthma, contributing to morbidity and mortality in the disease. Goblet cells are major mucus-producing cells, and goblet cell hyperplasia (GCH) is one feature of airway remodeling, defined as structural changes occurring in the airway. A number of studies have demonstrated that Th2-type cells play critical roles in this process and that particularly interleukin-13 (IL-13), among Th2-type cytokines, is a central mediator for GCH. However, the mechanism underlying how Th2 cytokines induce mucus production or GCH is poorly understood. Mouse calcium-activated chloride channel-3 (mCLCA-3; gob-5)/human CLCA-1 acts as a downstream molecule of Th2 cytokines, IL-4/IL-9/IL-13 signals, playing an important role in mucus production. Moreover, we have recently found that pendrin, an anion transporter, is induced by IL-13 and causes mucus production in airway epithelial cells. It is hoped that if we can clarify how mucus is produced, this will lead to development of novel therapeutic reagents to suppress mucus production in bronchial asthma.
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Cite this article as:
Izuhara K., Ohta S., Shiraishi H., Suzuki S., Taniguchi K., Toda S., Tanabe T., Yasuo M., Kubo K., Hoshino T. and Aizawa H., The Mechanism of Mucus Production in Bronchial Asthma, Current Medicinal Chemistry 2009; 16 (22) . https://dx.doi.org/10.2174/092986709788803196
DOI https://dx.doi.org/10.2174/092986709788803196 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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