Abstract
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.
Highlights
Bronchial allergic asthma is a prevalent disease and is increasing in developed countries
Allergen challenge or transgenic overexpression of IL-4 or IL-13 in mice resulted in pulmonary inflammation and goblet cell metaplasia, which was associated with significant inhibition of FOXa2 expression in the airway epithelium [38]
Interaction among dendritic cells (DCs), respiratory epithelium and environmental factors being responsible for goblet cell responses in the development of inflammatory Th2 cells (Figure 3B) in airway allergy will be introduced [88] other than regulatory Th2 cells, which are already mentioned
Summary
Bronchial allergic asthma (asthma) is a prevalent disease and is increasing in developed countries. Helper T(Th) cells play a fundamental role in both immediate and late reactions. Immediate reaction is induced by IgE-mediated increased mast cell response, whereas late response is characterized by recruitment of eosinophils, basophils, and Th2 cells producing cytokines such as IL4, a switch factor for IgE synthesis, and IL-5, an eosinophil growth factor [3]. Goblet cells in the airway epithelium at autopsy were demonstrated to be 30-fold higher in patients with fatal asthma than those with asthma who died of other causes [5]. Goblet cell responses in asthma play an important role in the pathogenesis of asthma (Figure 1). Molecular and animal-model studies have revealed several cellular events including inflammatory helper Th2 cytokines that are involved in the progression of asthma, leading to goblet cell responses. This article focusses on goblet cells and introduces molecular mechanisms of goblet cell metaplasia, differentiation and hyperplasia in asthma (Figures 2A and 2B)
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