Smoking as a risk factor which activates IL-2 gene polymorphism in patients with MDR-TB

Background: Determine IL-2 gene polymorphism(PM)in smokers with MDR-TB in lungs on the background of the respective cytokine production of blood. Methods .The study included 170 people in Kharkiv region of Ukraine including 60patients with MDR-TB and smoking (1 st group(g)),36-without MDR-TBand smoking(2 nd g),14-with MDR-TB and non-smoking(3 rd g)30-without MDR-TB and non-smoking(4 th g) and 30 healthy donors(5 th g).Studied promoter region T-330G of IL-2gene. Results. In the1 st g the levels ofIL-2 were (41.24±1.21),2 nd –(39.81±1.17),3 rd –(31.19±1.90),4 th –(31.87±0.84)and5 th –(21.60±0.80)pg/L.Differences between groups were significant (p th g was 60%compared to patients with TB:1 st g-5%,2 nd -13.89%,3 rd -14.29% and 4 th -16.67%.Heterozygous genotype IL-2 was observed in 76.67% in 1 st ,45.71% in 2 nd ,35.71% in the 3 rd ,13.33% in 4 th and 16.66% in 5 th g.Mutation homozygous genotype IL-2 was 18.33% in the 1 st g,in2 nd -41.67%,3 rd -50%,4 th -70%and5 th -3,34%.Differences between the 1 st and3 rd ,2 nd and4 th ,TBpatients and 5 th g were significant(p Conclusion. Smoking contributes to significant activation PM T-330G gene IL-2 heterozygous type that may lead to changes in the immune system making susceptible to MDR-TB.Compared to healthy controls patients with TB had significantly increased levels of serum IL-2.This coincided with greater frequency of heterozygous PM T-330Gof IL-2gene.In addition, these studies revealed a significant influence of the PM T-330GgeneIL-2(with PM IL-4andIL-10genes,which we also studied)on the changes in the population of Th-lymphocytes,clinical symptoms,relapse of TB,formation destructions in the lung,which may treatment outcomes in patients with MDR-TB.