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Association of the FCN2 Gene Single Nucleotide Polymorphisms with Susceptibility to Pulmonary Tuberculosis.

Xu DD, Wang C, Jiang F, Wei LL, Shi LY, Yu XM, Liu CM, Liu XH, Feng XM, Ping ZP, Jiang TT, Chen ZL, Li ZJ, Li JC - PLoS ONE (2015)

Bottom Line: Ficolin-2 (FCN2) is an innate immune pattern recognition molecule that can activate the complement pathway, opsonophagocytosis, and elimination of the pathogens.There was strong linkage disequilibrium (r2 > 0.80, P < 0.0001) between 7 SNPs except the -602 G>A site.This study provides a novel idea for the prevention and control of TB transmission from a genetics perspective.

View Article: PubMed Central - PubMed

Affiliation: Institute of Cell Biology, Zhejiang University, Hangzhou 310058, P.R. China.

ABSTRACT
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 (r2 > 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.

No MeSH data available.


Related in: MedlinePlus

Haploview plot illustrating the linkage disequilibrium (LD) of the FCN2 variants.A: Linkage disequilibrium of 7 functional FCN2 single nucleotide polymorphism (SNPs) in the healthy controls. Block 1 represent the 2 SNPs (−557A>G and −64 A>C) completely linked. B: Linkage disequilibrium of 7 functional FCN2 SNPs in the pulmonary TB group. Block 1 represent the 3 SNPs (−557A>G, −64 A>C and +6424 G>T) completely linked. Open squares indicate a high degree of LD (LD coefficient D′ = 1) between pairs of markers. Numbers indicate the r2 value.
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pone.0138356.g002: Haploview plot illustrating the linkage disequilibrium (LD) of the FCN2 variants.A: Linkage disequilibrium of 7 functional FCN2 single nucleotide polymorphism (SNPs) in the healthy controls. Block 1 represent the 2 SNPs (−557A>G and −64 A>C) completely linked. B: Linkage disequilibrium of 7 functional FCN2 SNPs in the pulmonary TB group. Block 1 represent the 3 SNPs (−557A>G, −64 A>C and +6424 G>T) completely linked. Open squares indicate a high degree of LD (LD coefficient D′ = 1) between pairs of markers. Numbers indicate the r2 value.

Mentions: There were strong linkage disequilibrium (r2>0.80, P < 0.0001) between 7 SNPs of the FCN2 gene except the -602 G>A site. The -557 A>G and -64 A>C sites were completely linked in the control group, while the -557 A>G, -64 A>C and +6424 G>T sites were completely linked in the pulmonary TB group (Fig 2). The linkage disequilibrium maps were basically identical in the two groups.


Association of the FCN2 Gene Single Nucleotide Polymorphisms with Susceptibility to Pulmonary Tuberculosis.

Xu DD, Wang C, Jiang F, Wei LL, Shi LY, Yu XM, Liu CM, Liu XH, Feng XM, Ping ZP, Jiang TT, Chen ZL, Li ZJ, Li JC - PLoS ONE (2015)

Haploview plot illustrating the linkage disequilibrium (LD) of the FCN2 variants.A: Linkage disequilibrium of 7 functional FCN2 single nucleotide polymorphism (SNPs) in the healthy controls. Block 1 represent the 2 SNPs (−557A>G and −64 A>C) completely linked. B: Linkage disequilibrium of 7 functional FCN2 SNPs in the pulmonary TB group. Block 1 represent the 3 SNPs (−557A>G, −64 A>C and +6424 G>T) completely linked. Open squares indicate a high degree of LD (LD coefficient D′ = 1) between pairs of markers. Numbers indicate the r2 value.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4574923&req=5

pone.0138356.g002: Haploview plot illustrating the linkage disequilibrium (LD) of the FCN2 variants.A: Linkage disequilibrium of 7 functional FCN2 single nucleotide polymorphism (SNPs) in the healthy controls. Block 1 represent the 2 SNPs (−557A>G and −64 A>C) completely linked. B: Linkage disequilibrium of 7 functional FCN2 SNPs in the pulmonary TB group. Block 1 represent the 3 SNPs (−557A>G, −64 A>C and +6424 G>T) completely linked. Open squares indicate a high degree of LD (LD coefficient D′ = 1) between pairs of markers. Numbers indicate the r2 value.
Mentions: There were strong linkage disequilibrium (r2>0.80, P < 0.0001) between 7 SNPs of the FCN2 gene except the -602 G>A site. The -557 A>G and -64 A>C sites were completely linked in the control group, while the -557 A>G, -64 A>C and +6424 G>T sites were completely linked in the pulmonary TB group (Fig 2). The linkage disequilibrium maps were basically identical in the two groups.

Bottom Line: Ficolin-2 (FCN2) is an innate immune pattern recognition molecule that can activate the complement pathway, opsonophagocytosis, and elimination of the pathogens.There was strong linkage disequilibrium (r2 > 0.80, P < 0.0001) between 7 SNPs except the -602 G>A site.This study provides a novel idea for the prevention and control of TB transmission from a genetics perspective.

View Article: PubMed Central - PubMed

Affiliation: Institute of Cell Biology, Zhejiang University, Hangzhou 310058, P.R. China.

ABSTRACT
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 (r2 > 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.

No MeSH data available.


Related in: MedlinePlus