Correlation Between GSH-Px Pro198Leu, CAT-262C/T, MnSOD Ala16Val Gene Polymorphisms and Allergic Rhinitis

Abstract

isolation from Results: be statistically significant. For the -262 C/T polymorphism of the CAT gene; was concluded with 95% confidence that the presence of the T-allele increased the susceptibility to allergic rhinitis 27,064 times. This increase was found to be statistically significant. For Ala16Val polymorphism of the Mn-SOD gene; was concluded with 95% confidence that the presence of the Ala allele increased the susceptibility to allergic rhinitis 25,791 times. This increase was found to be statistically significant. Conclusion: A significant relationship was found between allergic rhinitis and the genotypes and the frequencies of alleles in the polymorphisms of the MnSOD and CAT genes. However, no significant relationship was found between allergic rhinitis and the polymorphisms of the GPx-1 gene. not only allows the Th2 cells in its own colon to proliferate, but also begins secreting its own characteristic cytokines such as interleukin-3 (IL-3), IL-4, IL-5, IL-13, and granulocyte macrophage colony-stimulating factor (GM-CSF) (6,7). IL-4 and IL-13 stimulate B-lymphocytes in circulation and cause their transformation into plasma cells. These plasma cells secrete allergen-specific IgE to which they are sensitized. These specific IgE antibodies bind to high affinity IgE receptors on circulating basophils and mast cells in tissues. IgE-bound mast cells that increase because of continuous allergen exposure pass into the epithelium and are degranulated by recognizing mucosal allergens (8). The products of this degranulation are Ready to Act mediators such as histamine, tryptase, chymase, quinogenase, heparin and other enzymes. Additionally, mast cells secrete new inflammatory mediators such as PGD 2 , tumor necrosis factor-alpha, sulfidopeptidyl leukotrienes LTC 4 , LTD 4 , and LTE 4 . These mediators lead to increased permeability and mucosal edema. These events occur within 1-2 minutes of allergen exposure and are called early phase allergic response (6). Late phase reactions occur because of infiltration with mast cells, basophils, neutrophils, eosinophils and mononuclear cells