The role of CRTH2 gen polymorphism in the childhood age atopic asthma

Atopic disorders are characterized by an increase in the Th2 types cytokines like IL-4, IL-5, IL-9 and IL-13 produced primarily by Th2 cells. Expression of the prostaglandin receptor, such as CRTH2 "Chemoattractant receptor homologous molecule expressed on Th2", is critical for the secretion of these cytokines. In addition, the recently development of CRTH2 antagonists (Setipiprant, AZD1981, QAW039) are thought to be important therapeutic options for the control of asthma and maintenance of lung function in the future. In this study, we aim to figüre out the relationship between asthma and CRTH2 gene (G1544C, A1651G) polymorphism in childhood asthma and inflammatory events and we also investigated to determine the possibility of using CRTH2 antagonists for treatment in Turkish children. The study and control groups consisted of 143 patients (82 males/61 females) and 100 participants (36 males/64 females), with a mean age 8±3.5 and 30 ± 6.9 years, respectively. When the results of CRTH2 G1544C gene polymorphism of the patients in the patient group are examined; 48 (%33.6) patients were heterozygous (C/G), 13 (%9.1) were homozygous (C/C) and 82 (%57.3) patients were normal (G/G) genotype. The results for CRTH2 A1651G gene polymorphism of the patient group are examined; 45 (%31.5) patients were heterozygous (G/A), 6 (%4.2) patients were homozygous (G/G) and 92 (%64.3) patients were normal (A/A) genotype. When the control group was evaluated for CRTH2 G1544C polymorphism, 44 (%44) cases were heterozygous (C/G), 11 (%11) were homozygous (C/C) and 45 (%45) cases were normal (G/G) genotype. The results of the CRTH2 A1651G gene polymorphism were examined in the control group, normal (A/A) genotype was detected in 71 (%71) cases, heterozygous (G/A) 26 (%26) and homozygous (G/G) was 3 (%3) cases. İndividuals in both groups were compared, there were no statistically significant difference in gene polymorphism, allele distribution, atopy, family history as well as asthma weight and asthma control levels in both groups the difference was found to be statistically insignificant. As a result, there was no statistical difference in CRTH2 gene polymorphism (G1544C, A1651G) between asthmatic children and controls. These results suggests that CRTH2 gene polymorphisms are not strong effect on the pathogenesis of allergic asthma and genetic risk factor susceptibility to asthma in Turkish children. In addition, the results of our study did not provide us with strong scientific evidence that CRTH2 antagonist drugs, which have been tried to be developed for asthma therapy, would not be a suitable treatment option for Turkish children. However, we consider, studies which are also included in cytokines are needed to better understand the relation between CRTH2 and asthma with larger groups.