Polymorphisms in SIGLEC1 contribute to susceptibility to pulmonary active tuberculosis possibly through the modulation of IL-1β

被引:12
作者
de Lima, Dhemerson Souza [1 ]
Nunes, Vinicius C. L. [1 ]
Ogusku, Mauricio M. [2 ]
Sadahiro, Aya [3 ]
Pontillo, Alessandra [1 ]
Alencar, Bruna de Cunha [4 ]
机构
[1] Univ Sao Paulo, Inst Ciencias Biomed, Dept Imunol, Lab Imunogenet, Sao Paulo, SP, Brazil
[2] Inst Nacl de Pesquisas da Amazonia, Lab Micobacteriol, Manaus, AM, Brazil
[3] Univ Fed Amazonas, Dept Parasitol, Lab Imunol Mol, Manaus, AM, Brazil
[4] Univ Sao Paulo, Inst Ciencias Biomed, Dept Imunol, Lab Biol Celular Sistema Imune, Sao Paulo, SP, Brazil
基金
巴西圣保罗研究基金会;
关键词
Tuberculosis; SIGLEC1/CD169; SNPs; IL-1; beta; INNATE IMMUNE-RESPONSE; TRANSCRIPTIONAL SIGNATURE; CIRCULATING MONOCYTES; RECEPTOR; HEMAGGLUTININ; SIALOADHESIN; SUPPRESSES; EXPRESSION; RESIDENT; DISEASE;
D O I
10.1016/j.meegid.2017.09.031
中图分类号
R51 [传染病];
学科分类号
100401 ;
摘要
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-1 beta than non-carriers, suggesting the possible involvement of Siglec-1 signalling pathway with inflammasome complex.
引用
收藏
页码:313 / 317
页数:5
相关论文
共 28 条
[1]   Innate Immune Gene Polymorphisms in Tuberculosis [J].
Azad, Abul K. ;
Sadee, Wolfgang ;
Schlesinger, Larry S. .
INFECTION AND IMMUNITY, 2012, 80 (10) :3343-3359
[2]   An interferon-inducible neutrophil-driven blood transcriptional signature in human tuberculosis [J].
Berry, Matthew P. R. ;
Graham, Christine M. ;
McNab, Finlay W. ;
Xu, Zhaohui ;
Bloch, Susannah A. A. ;
Oni, Tolu ;
Wilkinson, Katalin A. ;
Banchereau, Romain ;
Skinner, Jason ;
Wilkinson, Robert J. ;
Quinn, Charles ;
Blankenship, Derek ;
Dhawan, Ranju ;
Cush, John J. ;
Mejias, Asuncion ;
Ramilo, Octavio ;
Kon, Onn M. ;
Pascual, Virginia ;
Banchereau, Jacques ;
Chaussabel, Damien ;
O'Garra, Anne .
NATURE, 2010, 466 (7309) :973-U98
[3]   Sialic acid-binding Ig-like lectin I expression in inflammatory and resident monocytes is a potential biomarker for monitoring disease activity and success of therapy in systemic lupus erythematosus [J].
Biesen, Robert ;
Demir, Cemal ;
Barkhudarova, Fidan ;
Gruen, Joachim R. ;
Steinbrich-Zoellner, Marta ;
Backhaus, Marina ;
Haeupl, Thomas ;
Rudwaleit, Martin ;
Riemekasten, Gabriela ;
Radbruch, Andreas ;
Hiepe, Falk ;
Burmester, Gerd-Ruediger ;
Gruetzkau, Andreas .
ARTHRITIS AND RHEUMATISM, 2008, 58 (04) :1136-1145
[4]  
Bogie J.F., 2017, MULT SCLER
[5]  
Bukvic B.K., PEDIAT ALLERGY IMMUN, V24, P10
[6]   MOUSE MACROPHAGE HEMAGGLUTININ (SHEEP ERYTHROCYTE RECEPTOR) WITH SPECIFICITY FOR SIALYLATED GLYCOCONJUGATES CHARACTERIZED BY A MONOCLONAL-ANTIBODY [J].
CROCKER, PR ;
GORDON, S .
JOURNAL OF EXPERIMENTAL MEDICINE, 1989, 169 (04) :1333-1346
[7]  
CROCKER PR, 1990, BLOOD, V76, P1131
[8]   Inflammasome genetics contributes to the development and control of active pulmonary tuberculosis [J].
de Lima, D. Souza ;
Ogusku, M. M. ;
Sadahiro, A. ;
Pontillo, A. .
INFECTION GENETICS AND EVOLUTION, 2016, 41 :240-244
[9]   A Type I Interferon Transcriptional Signature Precedes Autoimmunity in Children Genetically at Risk for Type 1 Diabetes [J].
Ferreira, Ricardo C. ;
Guo, Hui ;
Coulson, Richard M. R. ;
Smyth, Deborah J. ;
Pekalski, Marcin L. ;
Burren, Oliver S. ;
Cutler, Antony J. ;
Doecke, James D. ;
Flint, Shaun ;
McKinney, Eoin F. ;
Lyons, Paul A. ;
Smith, Kenneth G. C. ;
Achenbach, Peter ;
Beyerlein, Andreas ;
Dunger, David B. ;
Clayton, David G. ;
Wicker, Linda S. ;
Todd, John A. ;
Bonifacio, Ezio ;
Wallace, Chris ;
Ziegler, Anette-G. .
DIABETES, 2014, 63 (07) :2538-2550
[10]   Tuberculosis [J].
Frieden, TR ;
Sterling, TR ;
Munsiff, SS ;
Watt, CJ ;
Dye, C .
LANCET, 2003, 362 (9387) :887-899