Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/23657
Title: MBL2 gene polymorphisms and susceptibility to tuberculosis in a northeastern Brazilian population
Authors: Cruz, Heidi Lacerda Alves da
Silva, Ronaldo Celerino da
Segat, Ludovica
Carvalho, Márcia Schneider Zuzarte de Mendonça Gomes de
Brandão, Lucas André Cavalcanti
Guimarães, Rafael Lima
Santos, Fabiana Cristina Fulco
Lira, Laís Ariane Siqueira de
Montenegro, Lilian Maria Lapa
Schindler, Haiana Charifker
Crovella, Sergio
Affilliation: Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Departamento de imunologia. Recife, PE, Brasil.
Federal University of Pernambuco. Department of Genetics. Recife, PE, Brazil / Federal University of Pernambuco. Laboratory of Immunopathology Keizo Asami. Recife, PE, Brazil.
Institute for Maternal and Child Health. Trieste, Italy.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Departamento de imunologia. Recife, PE, Brasil / Federal University of Pernambuco. Department of Genetics. Recife, PE, Brazil.
Federal University of Pernambuco. Laboratory of Immunopathology Keizo Asami. Recife, PE, Brazil / Federal University of Pernambuco. Department of Pathology. Recife, PE, Brazil.
Federal University of Pernambuco. Department of Genetics. Recife, PE, Brazil / Federal University of Pernambuco. Laboratory of Immunopathology Keizo Asami. Recife, PE, Brazil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Departamento de imunologia. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Departamento de imunologia. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Departamento de imunologia. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Departamento de imunologia. Recife, PE, Brasil.
Institute for Maternal and Child Health. Trieste, Italy.
Abstract: The innate immune system represents the first line of host defense against pathogens. Genetics factors regulating the immune responses play a role in the susceptibility to infectious diseases, such as tuberculosis (TB). We analyzed MBL2 promoter and exon 1 functional single nucleotide polymorphisms (SNPs) in a group of 155TB patients and 148 healthy controls in order to evaluate their influence on the onset of infection and TB development. There was no association between MBL2 -550 HL promoter polymorphisms and susceptibility to develop TB, but heterozygous -221 Y/X genotype was significantly more frequent in pulmonary TB patients than controls. Moreover, MBL2 exon 1 O allele, was significantly associated with susceptibility to TB development in general (p=0.023, OR=1.61, 95% CI 1.05-2.49) and pulmonary TB (p=0.0008, OR=2.16, 95% CI 1.35-3.46); C allele at codon 57, as well as A/C genotype, were significantly more frequent in TB patients than in controls. Our results indicate that MBL2 polymorphisms, especially at codon 57, could be considered as risk factors for TB development.
Keywords: Tuberculosis
Innate immunity
MBL2
Pulmonary
Polymorphisms
keywords: Tuberculose
Imunidade inata
MBL2
Pulmonar
Polimorfismos
DeCS: Predisposição Genética para Doença
genética
Lectina de Ligação a Manose
genética
Adolescente
Adulto
Brasil
epidemiologia
Estudos de Casos e Controles
Feminino
Genótipo
Humanos
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único
genética
Tuberculose Pulmonar
epidemiologia
Tuberculose Pulmonar
genética
Adulto Jovem
Issue Date: 2013
Citation: CRUZ, H. L. A. da et al. MBL2 gene polymorphisms and susceptibility to tuberculosis in a northeastern Brazilian population. Infection, Genetics and Evolution: Journal of Molecular Epidemiology and Evolutionary Genetics in Infectious Diseases, v. 19, p. 323–329, out. 2013.
DOI: 10.1016/j.meegid.2013.03.002
ISSN: 1567-7257
Copyright: open access
Appears in Collections:PE - IAM - Artigos de Periódicos

Files in This Item:
File Description SizeFormat 
art. MBL2 gene polymorphisms - cruz.pdf265.36 kBAdobe PDFView/Open


FacebookTwitterDeliciousLinkedInGoogle BookmarksBibTex Format mendeley Endnote DiggMySpace

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.