Deo Kabuye1, Yang Chu1, Wenting Lao1, Guojiang Jin1, Hui Kang2. 1. Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning Province, China. 2. Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning Province, China. Electronic address: kanghui65@sina.com.
Abstract
BACKGROUND: Pulmonary tuberculosis caused by an intracellular pathogen, Mycobacterium tuberculosis continues to exist as a hazardous disease to human life globally. Genetic polymorphisms regulate resistance and susceptibility to tuberculosis. The C-type lectin receptor of family 4 member E (CLEC4E) confers protection against tuberculosis in laboratory animals but its function in influencing exposure or resistance to pulmonary tuberculosis (PTB) in humans remains obscure. AIM: We conducted this research to analyze the effects or concomitance of CLEC4E gene variations with susceptibility to pulmonary tuberculosis in a northern Chinese population. METHOD: In this study, 202 participants with pulmonary tuberculosis and 214 controls without PTB were enrolled. Two single nucleotide polymorphisms (SNPs) for CLEC4E on chromosome 12 were selected with a minor allele frequency of >0.05. All the SNPs were genotyped using high resolution melting analysis-PCR. RESULTS: We estimated and compared two SNPs, rs10841845 and rs10841847. From our study findings, CLEC4E rs10841845 conferred protection against the development of pulmonary TB with a P value of <0.05 and odds ratio of <1 for all models of genetic inheritance. CLEC4E rs10841847 genotypes in co-dominant, Recessive, Dominant models and alleles had a significant statistical difference between patients and controls associated with resistance against the development of PTB (P<0.05 and OR<1). CONCLUSION: Our findings suggest that variations at rs10841845 and rs10841847 of CLEC4E genes are associated with increased individual protection against PTB.
BACKGROUND:Pulmonary tuberculosis caused by an intracellular pathogen, Mycobacterium tuberculosis continues to exist as a hazardous disease to human life globally. Genetic polymorphisms regulate resistance and susceptibility to tuberculosis. The C-type lectin receptor of family 4 member E (CLEC4E) confers protection against tuberculosis in laboratory animals but its function in influencing exposure or resistance to pulmonary tuberculosis (PTB) in humans remains obscure. AIM: We conducted this research to analyze the effects or concomitance of CLEC4E gene variations with susceptibility to pulmonary tuberculosis in a northern Chinese population. METHOD: In this study, 202 participants with pulmonary tuberculosis and 214 controls without PTB were enrolled. Two single nucleotide polymorphisms (SNPs) for CLEC4E on chromosome 12 were selected with a minor allele frequency of >0.05. All the SNPs were genotyped using high resolution melting analysis-PCR. RESULTS: We estimated and compared two SNPs, rs10841845 and rs10841847. From our study findings, CLEC4Ers10841845 conferred protection against the development of pulmonary TB with a P value of <0.05 and odds ratio of <1 for all models of genetic inheritance. CLEC4Ers10841847 genotypes in co-dominant, Recessive, Dominant models and alleles had a significant statistical difference between patients and controls associated with resistance against the development of PTB (P<0.05 and OR<1). CONCLUSION: Our findings suggest that variations at rs10841845 and rs10841847 of CLEC4E genes are associated with increased individual protection against PTB.
Authors: Jasmine M Olvany; Lindsay N Sausville; Marquitta J White; Alessandra Tacconelli; Gloria Tavera; Rafal S Sobota; Cinzia Ciccacci; Anders S Bohlbro; Christian Wejse; Scott M Williams; Giorgio Sirugo Journal: Infect Genet Evol Date: 2020-09-22 Impact factor: 3.342