TREM-1 modulation during early stages of dengue virus infection

被引:26
作者
Ruiz-Pacheco, J. A. [1 ,2 ]
Vivanco-Cid, H. [3 ]
Izaguirre-Hernandez, I. Y. [3 ]
Estrada-Garcia, I. [2 ]
Arriaga-Pizano, L. [4 ]
Chacon-Salinas, R. [2 ]
Fonseca-Coronado, S. [5 ]
Vaughan, G. [1 ]
Tovar, K. Ruiz [1 ]
Rivera-Osorio, M. P. [1 ]
Escobar-Gutierrez, A. [1 ]
机构
[1] Secretaria Salud Mexico, Inst Diagnost & Referencia Epidemiol, Dept Invest Inmunol, Mexico City, DF, Mexico
[2] IPN, Escuela Nacl Ciencias Biol, Dept Inmunol, Mexico City 07738, DF, Mexico
[3] Univ Veracruzana, Inst Invest Med Biol, Veracruz, Veracruz, Mexico
[4] Hosp Especialidades Ctr Med La Raza, Ctr Med Nacl Siglo XXI, Unidad Invest Med Inmunoquim, Mexico City, DF, Mexico
[5] Univ Nacl Autonoma Mexico, Fac Estudios Super Cuautitlan, Cuautitlan, Estado De Mexic, Mexico
关键词
Dengue virus; TREM-1; sTREM-1; Innate immunity; NECROSIS-FACTOR-ALPHA; MYELOID CELLS-1; EXPRESSION PATTERNS; HUMAN NEUTROPHILS; CUTTING EDGE; SOLUBLE FORM; SERUM-LEVELS; CHILDREN; SURFACE; ACTIVATION;
D O I
10.1016/j.imlet.2014.01.003
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Uncontrolled and intricate production of inflammatory factors is the characteristic feature of dengue infection. The triggering receptor expressed in myeloid cells-1 (TREM-1), expressed on the surface of monocytes and neutrophils, is capable of enhancing and regulating the inflammatory response via the production of different mediators in bacterial and viral infections. Here, both the expression of TREM-1 on human monocytes and neutrophils from peripheral blood of dengue infected individuals, as well as the levels of the soluble form of TREM-1 (sTREM-1) in the sera of these patients were compared against healthy controls. A significant reduction of TREM-1 expression was observed in neutrophils during the first days of infection, followed by a gradual recovery throughout the course of infection. Also, sera from DEN V-infected patients exhibited significantly higher sTREM-1 levels than healthy individuals. The difference was more pronounced during the first 5 days after the onset of symptoms. These findings highlight the dynamic process of TREM-1 expression during DENV infection. We hypothesized that increment of free sTREM-1 could be a compensatory mechanism aiming to counteract the inflammatory process elicited during DENV infection. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:183 / 188
页数:6
相关论文
共 44 条
[1]   Elevated serum levels of high mobility group box 1 (HMGB1) protein in dengue-infected patients are associated with disease symptoms and secondary infection [J].
Allonso, Diego ;
Belgrano, Fabricio S. ;
Calzada, Naifi ;
Guzman, Maria G. ;
Vazquez, Susana ;
Mohana-Borges, Ronaldo .
JOURNAL OF CLINICAL VIROLOGY, 2012, 55 (03) :214-219
[2]   Cathelicidin Peptide LL-37 Modulates TREM-1 Expression and Inflammatory Responses to Microbial Compounds [J].
Amatngalim, Gimano D. ;
Nijnik, Anastasia ;
Hiemstra, Pieter S. ;
Hancock, Robert E. W. .
INFLAMMATION, 2011, 34 (05) :412-425
[3]   The global distribution and burden of dengue [J].
Bhatt, Samir ;
Gething, Peter W. ;
Brady, Oliver J. ;
Messina, Jane P. ;
Farlow, Andrew W. ;
Moyes, Catherine L. ;
Drake, John M. ;
Brownstein, John S. ;
Hoen, Anne G. ;
Sankoh, Osman ;
Myers, Monica F. ;
George, Dylan B. ;
Jaenisch, Thomas ;
Wint, G. R. William ;
Simmons, Cameron P. ;
Scott, Thomas W. ;
Farrar, Jeremy J. ;
Hay, Simon I. .
NATURE, 2013, 496 (7446) :504-507
[4]   A role for triggering receptor expressed on myeloid cells-1 in host defense during the early-induced and adaptive phases of the immune response [J].
Bleharski, JR ;
Kiessler, V ;
Buonsanti, C ;
Sieling, PA ;
Stenger, S ;
Colonna, M ;
Modlin, RL .
JOURNAL OF IMMUNOLOGY, 2003, 170 (07) :3812-3818
[5]   Cutting edge: Inflammatory responses can be triggered by TREM-1, a novel receptor expressed on neutrophils and monocytes [J].
Bouchon, A ;
Dietrich, J ;
Colonna, M .
JOURNAL OF IMMUNOLOGY, 2000, 164 (10) :4991-4995
[6]   TREM-1 amplifies inflammation and is a crucial mediator of septic shock [J].
Bouchon, A ;
Facchetti, F ;
Weigand, MA ;
Colonna, M .
NATURE, 2001, 410 (6832) :1103-1107
[7]  
Butthep P, 1993, Southeast Asian J Trop Med Public Health, V24 Suppl 1, P246
[8]  
Chaturvedi UC, 1999, J MED VIROL, V59, P335, DOI 10.1002/(SICI)1096-9071(199911)59:3<335::AID-JMV13>3.0.CO
[9]  
2-E
[10]  
Chen HL, 2008, JPN J INFECT DIS, V61, P31