Essay --

As modern medical research begins to discover the deep-rooted genetic and environmental origins of many chronic diseases and illnesses, researchers have began to realize the complexity of illnesses that plague mankind. One prevalent disease among humans is Asthma, a chronic lung disease that irritates and tightens the airways, resulting in reocurring periods of coughing, chest tightness, shortness of breath, and wheezing. Asthma’s phenotypic range does not follow the relative simplicity of Mendelian genetics, but is rather rooted in multiple genes, such as Interleukin-13 (IL-13), and specific environmental exposures such as air pollution. The IL-13 gene is one of several hundred candidate genes which are segments of DNA believed to contain nucleotide sequences affecting the asthma phenotype. The IL-13 gene is mostly expressed in T Helper cell 2 (TH2) as Interleukin-13 cytokines, operating through IL-13R (a heterodimer of IL-4RÃŽ ± and IL-13RÃŽ ±1) (4, 11, 6). These cytokines relay messages to other immune cells, warranting a coordinated immune response (6). However, the operation of Interleukin-13 is largely dependent on the presence and expression of Interleukin-4 (IL-4), another cytokine (11). Not only is a dimer of IL-4, IL-4Ra, critical to the reception of IL-13 cytokines, but IL-14 is crucial in the advancement of T cells in Th2 cells, the main producer of IL-13 cytokines (11). This epistatic dependency of IL-13 on the expression of IL-4 and other genes is another contributor to the complexity of asthma. In addition to various genes affecting the phenotype of asthma, multiple environmental factors like indoor and outdoor air pollution, tobacco smoke, and allergies to pets, molds, common pests (e.g. cockroaches) change gene expr... ...on and a related treatment option (10). The severity of an indivual’s asthma is based on many factors, including the prescence and epistatic interactions of the asthma susceptibility genes; even if the genes are present, if the complementary miRNA strand is actively synthesized, the genes won’t cause asthma. Genetic and miRNA expression can then be altered by environmental exposures through methylation and acetylation. The genetic and environmental contributions discussed here to the expression of asthma are a small fraction of the known factors. Due to the complicated intertwined relationship of the abundant factors contributing toward asthmatic phenotypes that have been discovered in approximately the last twenty years, the currently known complexity of asthma could very well be simple in relation to the verity of asthma’s genetic and environmental labyrinthe.