IGHE and asthma: Recent molecular, cellular, and animal model studies have revealed that several cellular events are involved in the progression of asthma and in the subsequent injury to the tissues of the bronchial epithelium, including increased IgE synthesis, an imbalanced T helper-type 1/T helper-type 2 (Th1/Th2) paradigm, increased Th2 cytokines leading to the recruitment of inflammatory cells to the airway and the activation of those cells; increased production of reactive oxygen species (ROS); and mitochondrial damage and dysfunction in activated inflammatory cells [10,11].