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Abstract
AimWe performed a comprehensive meta-analysis to determine the association between P2X7 -762T/C polymorphism and pulmonary tuberculosis susceptibility.MethodologyBased on comprehensive searches of the PubMed, SCI, Elsevier, China National Knowledge Infrastructure (CNKI) and Wanfang Database, we identified eligible studies about the association between P2X7 -762T/C polymorphism and pulmonary tuberculosis risk. Pooled odds ratio (ORs) and 95% confidence intervals (95%CIs) were calculated in random-effects model.ResultsA total of 2207 tuberculosis cases and 2220 controls in 8 case-control studies were included in this meta-analysis. Allele model (C vs. T: p = 0.15; OR = 0.83, 95% CI = 0.65–1.07), homozygous model (CC vs. TT: p = 0.23; OR = 0.73, 95% CI = 0.44 to 1.22), and heterozygous model (CT vs. TT: p = 0.57; OR = 0.92, 95% CI = 0.68 to 1.24) did not show increased risk of developing pulmonary tuberculosis. Similarly, dominant model (CC+CT vs. TT: p = 0.32; OR = 0.84, 95% CI = 0.59 to 1.19) and recessive model (CC vs. CT+TT: p = 0.08; OR = 0.77, 95% CI = 0.57 to 1.04) failed to show increased risk of developing pulmonary tuberculosis. Subgroup analysis by ethnicity did not detect any significant association between P2X7–762T/C polymorphism and pulmonary tuberculosis susceptibility.Conclusions P2X7 -762T/C gene polymorphism is not associated with pulmonary tuberculosis susceptibility.
Highlights
Tuberculosis is caused by the bacillus Mycobacterium tuberculosis and remains a major challenge to global public health [1]
6 studies focused on the association between pulmonary tuberculosis risks and P2X7 -762T/C polymorphism while other studies enrolled both pulmonary tuberculosis and extra-pulmonary tuberculosis patients
There was a total of 2207 subjects with pulmonary tuberculosis 1442 subjects were diagnosed by culture, 479 subjects were diagnosed by smear, and the methods of diagnosis of the rest subjects were not reported (Table 1)
Summary
Tuberculosis is caused by the bacillus Mycobacterium tuberculosis and remains a major challenge to global public health [1]. According to the report of World Health Organization, there were an estimated 8.6 million incident case of tuberculosis and 1.3 million deaths in 2012 [2]. One-third of population is infected by Mycobacterium tuberculosis, only 10% of those develop clinical disease during their lifetime. Multiple factors contribute to the risk of infection and development of tuberculosis including environmental factors, host–pathogen interactions and genetic factors [3]. Epidemiological studies indicate that the risk of developing tuberculosis in human is strongly influenced by genetic factors [4]. Gene polymorphisms of SLC11A1 (formerly NRAMP1), vitamin D receptor, toll-like receptor 2, tumor necrosis factor-alpha and monocyte chemoattractant protein-1 have been identified to be associated with susceptibility of tuberculosis [5–9]
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