Studying the relationship between allergo-inflammation and left atrium and pulmonary vein pathological changes in allergic asthma.

Abstract

Allergic asthma is an inflammatory airway disease influenced by genetic and environmental factors and orchestrated by imbalance between T helper 1 cell (Th1) and two immune responses. Inflammation contributes to pathological changes and remodeling in tissues such as the vascular, lung, heart, and beds. The purpose for this study was to evaluate the effects of allergic asthma on heart pathology and remodeling. In methodology, mice were allocated into two healthy and asthma groups, followed by the assessment of airway hyperresponsiveness (AHR), cell enumeration in bronchoalveolar lavage fluid (BALF), measurement of interleukin (IL)-4, IL-33, IL-5, interferon gamma (IFN-γ), and IL-13, total immunoglobulin E (IgE) levels, and analysis of remodeling factors. Also, gene expression analysis was performed for troponin, suppressor of mothers against decapentaplegic (SMAD)2, myocyte enhancer factor 2 (MEF-2), and SMAD3. Finally, histopathological study was conducted. The result revealed that asthma induction augmented AHR and elevated eosinophil percentage, elevated the levels of IL-13, IL-33, IL-5, IL-4, IgE, Helicobacter pylori (HP), and transforming growth factor beta (TGF-β), and the gene expression of SMAD3. Also, eosinophilic inflammation, goblet cell meta/hyperplasia, and mucus secretion were increased in asthmatic versus healthy mice. The level of IFN-γ was lower in the asthma compared to the control group; however, the expressions of troponin, SMAD2, and MEF-2 genes showed no significant differences. It was concluded that allergic asthma changed the balance between type 1 and 2 cytokines, which could possibly lead to profound effects on the cardiovascular system's structure and/or function.