Asthma is an inflammatory disorder of the airways, and the airway epithelium has the central role in its pathogenesis. In general, the airway inflammation is characterised by the infiltration of the epithelium and submucosa by a range of inflammatory cells driven largely by Th-2 lymphocytes, eosinophils, and mast cells. The pathogenic mechanisms of nonatopic asthma in comparison to its atopic counterpart have always been a subject of debate. Although clinically are two distinct entities, more similarities than differences have been observed between the two in terms of immunopathogenesis, underlying IgE mechanisms, and so on. in a number of previous studies. More information has become available in recent years comparing the ultrastructure of the epithelium in these two types of asthma. A comparison of airway epithelium in atopic and nonatopic asthma is presented here from the available information in the literature. Similarities outnumber the differences, until we unravel the mystery surrounding these two important phenotypes of asthma in more detail. 1. Introduction Asthma is a common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airflow obstruction, bronchial hyper responsiveness, and underlying inflammation [1]. Asthma may be classified clinically on the basis of various parameters including the atopic status of the individual, the degree of airway obstruction, or the nature of trigger factors. By convention, the classification into atopic or nonatopic asthma is based on the presence or absence of clinical symptoms precipitated by one or more common aeroallergens, supported by the presence of allergen-specific antibodies as evidenced by skin prick +/？ serological tests. The airways epithelium likely plays a key role in the pathogenesis of asthma, as it is a key interface with the external environment. There is ongoing debate as to whether atopic and nonatopic asthma are immunopathologically two distinct entities or if both are driven by similar mechanisms, and the answer to this question is still not clear. The entity of intrinsic or nonatopic asthma continues to raise questions about the possible role of IgE-mediated mechanisms in asthma pathogenesis. The clarification of this issue becomes more relevant with the current availability of anti-IgE therapy for the treatment of atopic asthma. The main theme of this paper is to address airway epithelium as central to the theatre of asthmatic inflammation and to compare the airways microenvironment in atopic and nonatopic asthma. 2. Airway Epithelium
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