文献类型：期刊文献

英文题名：Association of the FCN2 Gene Single Nucleotide Polymorphisms with Susceptibility to Pulmonary Tuberculosis

作者：Xu, Dan-Dan[1];Wang, Chong[1];Jiang, Feng[2];Wei, Li-Liang[3];Shi, Li-Ying[4];Yu, Xiao-Mei[4];Liu, Chang-Ming[1];Liu, Xue-Hong[5];Feng, Xian-Min[6];Ping, Ze-Peng[1];Jiang, Ting-Ting[1];Chen, Zhong-Liang[1];Li, Zhong-Jie[1];Li, Ji-Cheng[1]

机构：[1]Zhejiang Univ, Inst Cell Biol, Hangzhou 310058, Zhejiang, Peoples R China;[2]Beijing Univ Chinese Med, Dongzhimen Hosp, Beijing 100700, Peoples R China;[3]Sixth Hosp Shaoxing, Dept Resp Med, Shaoxing 312000, Peoples R China;[4]Zhejiang Hosp, Dept Clin Lab, Hangzhou 310013, Zhejiang, Peoples R China;[5]Shaoxing Univ, Sch Med, Shaoxing 312000, Peoples R China;[6]Jilin Med Coll, Sch Lab Med, Jilin 132013, Peoples R China

年份：2015

卷号：10

期号：9

外文期刊名：PLOS ONE

收录：SCI-EXPANDED(收录号：WOS:000361769400087)、、WOS

基金：This work was supported by the following sources of funding: 1. National Special Sci-Tech Projects (No. 2012ZX10005001-006; http://www.most.gov.cn/; LJC); 2. National Basic Research Program of China (No. 2014CB543002; http://www.most.gov.cn/; LJC); 3. National Natural Science Foundation of China (No. 81273882; http://www.nsfc.gov.cn/; LJC); 4. Medical & hygienic Foundation of Zhejiang Province (No. 2013KYA209; http://www.zjwst.gov.cn/; WLL); and 5. Education Department of Jilin Province (No. 2014367; http://www.jledu.gov.cn/jyt/; FXM). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

语种：英文

外文摘要：Ficolin-2 (FCN2) is an innate immune pattern recognition molecule that can activate the complement pathway, opsonophagocytosis, and elimination of the pathogens. The present study aimed to investigate the association of the FCN2 gene single nucleotide polymorphisms (SNPs) with susceptibility to pulmonary tuberculosis (TB). A total of seven SNPs in exon 8 (+6359 C>T and +6424 G>T) and in the promoter region (-986 G>A, -602 G>A, -557 A>G, -64 A>C and -4 A>G) of the FCN2 gene were genotyped using the PCR amplification and DNA sequencing methods in the healthy controls group (n = 254) and the pulmonary TB group (n = 282). The correlation between SNPs and pulmonary TB was analyzed using the logistic regression method. The results showed that there were no significant differences in the distribution of allelic frequencies of seven SNPs between the pulmonary TB group and the healthy controls group. However, the frequency of the variant homozygous genotype (P = 0.037, -557 A>G; P = 0.038, -64 A>C; P = 0.024, +6424 G>T) in the TB group was significantly lower than the control group. After adjustment for age and gender, these variant homozygous genotypes were found to be recessive models in association with pulmonary TB. In addition, -64 A>C (P = 0.047) and +6424 G>T (P = 0.03) were found to be codominant models in association with pulmonary TB. There was strong linkage disequilibrium (r(2) > 0.80, P < 0.0001) between 7 SNPs except the -602 G>A site. Therefore, -557 A>G, -64 A>C and +6424 G>T SNPs of the FCN2 gene were correlated with pulmonary TB, and may be protective factors for TB. This study provides a novel idea for the prevention and control of TB transmission from a genetics perspective.