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Title: | Polymorphisms in SIGLEC1 contribute to susceptibility to pulmonary active tuberculosis possibly through the modulation of IL-1ß |
Authors: | Lima, Dhêmerson Souza de Leal, Vinicius Nunes Cordeiro Ogusku, Maurício Morishi Sadahiro, Aya Pontillo, Alessandra Alencar, Bruna C. de |
Keywords: | Inflammasome Interleukin-1beta Interleukin-1beta Sialoadhesin Siglec1 Protein, Human Adult Cohort Analysis Controlled Study Cytokine Production Disease Association Female Gene Gene Frequency Genetic Association Genetic Susceptibility Genotype Heterozygote Human Human Cell Lung Tuberculosis Major Clinical Study Male Priority Journal Siglec1 Gene Signal Transduction Polymorphism, Single Nucleotide Allele Case Control Study Gene Linkage Disequilibrium Genetic Predisposition Genetics Lung Tuberculosis Metabolism Microbiology Middle Aged Mycobacterium Tuberculosis Young Adult Adult Alleles Case-control Studies Female Genetic Predisposition To Disease Genotype Humans Interleukin-1beta Linkage Disequilibrium Male Middle Aged Mycobacterium Tuberculosis Polymorphism, Single Nucleotide Sialic Acid Binding Ig-like Lectin 1 Tuberculosis, Pulmonary Young Adult |
Issue Date: | 2017 |
metadata.dc.publisher.journal: | Infection, Genetics and Evolution |
metadata.dc.relation.ispartof: | Volume 55, Pags. 313-317 |
Abstract: | Siglec-1/CD169 is a sialoadhesin expressed by macrophages thought to function in cell-to-cell interactions. In the lung, the expression of Siglec-1 is specific for alveolar macrophages and single nucleotide polymorphisms (SNPs) in SIGLEC1 have been recently associated with asthma severity. Taking in account the role of alveolar macrophages in the control of M. tuberculosis and the poor literature about the contribution of SIGLEC1 genetics in M. tuberculosis susceptibility and development of pulmonary active TB, selected SNPs in SIGLEC1 were analysed in a case/control cohort from a TB endemic area of Brazil Amazon. Our findings evidenced for the first time the novel association between SIGLEC1 rs3859664 SNP and active pulmonary TB. Intriguingly, carriers of the polymorphism produced less IL-1ß than non-carriers, suggesting the possible involvement of Siglec-1 signalling pathway with inflammasome complex. © 2017 Elsevier B.V. |
metadata.dc.identifier.doi: | 10.1016/j.meegid.2017.09.031 |
Appears in Collections: | Artigos |
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