Open AccessDeletion polymorphism of GSTT1 gene as protective marker for allergic rhinitis
Author(s) -
Iorio Andrea,
Polimanti Renato,
Piacentini Sara,
Liumbruno Giancarlo Maria,
Manfellotto Dario,
Fuciarelli Maria
Publication year - 2015
Publication title -
the clinical respiratory journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.789
H-Index - 33
eISSN - 1752-699X
pISSN - 1752-6981
DOI - 10.1111/crj.12170
Subject(s) - medicine , gene , immunology , polymorphism (computer science) , genetics , genotype , biology
Background and Aims Allergic rhinitis ( AR ) is one of the most common respiratory diseases among human populations. Strong evidence suggests that genetic predisposition and environmental factors could contribute to the development of this complex disease. Glutathione S ‐transferases ( GSTs ) are biomarkers of inflammation and oxidative stress. These phase II enzymes play a significant role in detoxifying xenobiotic compounds. To analyze the role of GST gene polymorphisms in AR pathogenesis in a case‐control population of 103 patients affected by AR and 200 healthy non‐allergic subjects. Methods We screened genomic DNA extracted from buccal cells for GSTM1 positive/null, GSTP1 * I 105 V (rs1695) and GSTT1 positive/null polymorphisms. The X 2 ‐test, odds ratio ( OR ) and logistic regression were used as statistical analyses. Results Significant differences in null genotype distribution between AR patients (13%) and healthy controls (30%) were found for the GSTT1 null genotype ( OR = 0.30, 95% confidence interval = 0.14–0.65; P = 0.001). GSTM1 and GSTP1 polymorphisms did not show any significant results. Conclusion Our data indicated that GSTT1 may be a susceptibility locus for AR . Specifically, the positive/null polymorphism of GSTT1 may be involved in an oxidative stress‐related mechanism that may enhance pathogenic pathways related to AR . Moreover, beside GSTT1 , this deletion polymorphism affects also another gene potentially related to AR phenotype, LOC 391322 . This gene belongs to MIF (macrophage migration inhibitory factor) gene family and several studies indicated the role of this gene in several immunology‐related phenotypes. Therefore, two different scenarios may explain the observed genetic association.