%0 Journal Article
%T Ultrastructural Changes of Airway in Murine Models of Allergy and Diet-Induced Metabolic Syndrome
%A Geeta Devi Leishangthem
%A Ulaganathan Mabalirajan
%A Vijay Pal Singh
%A Anurag Agrawal
%A Balaram Ghosh
%A Amit Kumar Dinda
%J ISRN Allergy
%D 2013
%R 10.1155/2013/261297
%X Studying ultrastructural changes could reveal novel pathophysiology of obese-asthmatic condition as existing concepts in asthma pathogenesis are based on the histological changes of the diseased airway. While asthma is defined in functional terms, the potential of electron microscopy (EM) in providing cellular and subcellular detail is underutilized. With this view, we have performed transmission EM in the lungs from allergic mice that show key features of asthma and high-fat- or high-fructose-fed mice that mimicked metabolic syndrome to illustrate the ultrastructural changes. The primary focus was epithelial injury and metaplasia, which are cardinal features of asthma and initiate airway remodeling. EM findings of the allergically inflamed mouse lungs correlate with known features of human asthma such as increased mitochondria in airway smooth muscle, platelet activation and subepithelial myofibroblasts. Interestingly, we found a clear and unambiguous evidence to suggest that ciliated cells can become goblet cells using immunoelectron microscopy. Additionally, we show for the first time the stressed mitochondria in the bronchial epithelia of high-fat- or high-fructose-fed mice even without allergen exposure. These results may stimulate interest in using EM in understanding novel pathological mechanisms for different subtypes of asthma including obese asthma. 1. Introduction Asthma, a chronic airway disease, is characterized by reversible airflow obstruction, airway inflammation, airway hyperresponsiveness (AHR), and structural changes referred to as airway remodeling [1, 2]. Asthma can be described in clinical, physiological, immunological, and pathological terms, each providing its own unique context in understanding asthma pathogenesis. Though this description seems to be simple, various endotypes/phenotypes of asthma have been recently demonstrated indicating the complexity of asthma [3¨C5]. Similar complexity also exists in the responsiveness to available antiasthma medications. The difficult-to-treat or severe or refractory asthmatics are responsible for significant health and economic burden of asthma even though they are just 10% of all asthmatics [6¨C9]. In this context, it has been demonstrated that asthma severity correlates very well with increased body mass index [10, 11]. As obese-asthmatic condition does not fall in the description of general asthma, there is necessity to understand the novel mechanisms for this condition. Muscular disease, inflammation dominant disease, airway remodeling, and epithelial injury are the historical
%U http://www.hindawi.com/journals/isrn.allergy/2013/261297/