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.
Highlights
Tuberculosis (TB) is a chronic infectious disease caused by Mycobacterium tuberculosis (Mtb)
The present study aimed to investigate the association of the FCN2 gene single nucleotide polymorphisms (SNPs) with susceptibility to pulmonary tuberculosis (TB)
The frequency of GG genotype at -557 A>G site in the pulmonary TB group (0.010) was lower than the control group (0.040), and there was a significant difference between the two groups (P = 0.037; Odds ratios (OR) = 0.271; 95% confidence intervals (CI), 0.073–1.003)
Summary
Tuberculosis (TB) is a chronic infectious disease caused by Mycobacterium tuberculosis (Mtb). According to the World Health Organization’s 2013 global report on TB, an estimated 9.0 million people developed TB and 1.5 million died from this disease, 360,000 of whom were HIV-positive [2]. Single nucleotide polymorphisms (SNPs) in genes as inducible nitric oxide synthase [9, 10], solute carrier protein 11A1 [11], Toll-like receptors [12, 13], nucleotide oligomerization domain 2 [14], CD14 [15], vitamin D nuclear receptor [16], mannose-binding lectin [17], surfactant protein A [18], tumor necrosis factor [19], interleukin (IL)-6 [20] and IL-10 [21], monocyte chemoattractant protein-1 [22], RANTES [23] and C-X-C motif chemokine 10 [24] have been reported [25] to be associated with increased or decreased risk of developing TB
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