American Journal of Immunology

LEUKOTRIENE C4 SYNTHASE AND LEUKOTRIENE RECEPTOR-1 GENES POLYMORPHISM AMONG ATOPIC ASTHMATIC PATIENTS

Heba M. Kadry, Amal H. Atta, Mostafa K. Sultan and Nagwa A. El-Baz

DOI : 10.3844/ajisp.2014.63.72

American Journal of Immunology

Volume 10, Issue 2

Pages 63-72

Abstract

Asthma is a complex polygenic disease in which Cysteinyl Leukotrienes (Cys-LTs) are a potential risk factors causing airway inflammation and remodeling, which are characteristics of asthma. The polymorphisms in the leukotriene C4 synthase -444A/C and cysteinyl leukotriene receptor1 927 T/C genes has been implicated in susceptibility to asthma. The objective of this study was to analyse two different polymorphisms, LTC4S-444 A/C and Cys-LTR1 927 T/C single nucleotide polymorphism and to determine whether there is an association between these polymorphisms and asthma development. The study included two groups (30 asthmatics and 30 healthy controls). They were genotyped for the LTC4S-444 A/C and CysLTR1 927 T/C polymorphisms by PCR-RFLP. Their total serum IgE levels and urinary LTE4 levels were measured by Enzyme Linked Immunosorbent Assay (ELISA). IgE levels and urinary leukotriene E4 levels were higher in patient group than control group. The genotype and allele frequencies of both LTC4S-444 A/C and CysLTR1 927 T/C polymorphism were not significantly different between asthmatic patients and control group. While urinary leukotriene E4 levels were significantly higher in variant types of LTC4 synthase (AC and CC) compared to wild type (AA). This study does not support the role of these polymorphisms in genetic susceptibility to asthma but provide an evidence for a functional role of LTC4 synthase-444 A/C polymorphism on Cys-LT synthesis.

Copyright

© 2014 Heba M. Kadry, Amal H. Atta, Mostafa K. Sultan and Nagwa A. El-Baz. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.