TREM-1 modulation during early stages of dengue virus infection.
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 DENV-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.
Departamento de Investigaciones Inmunológicas, Instituto de Diagnóstico y Referencia Epidemiológicos, Secretaría de Salud, México, DF, México; Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, IPN, México, DF, México.
J A
JA
Ruiz-Pacheco
Instituto de Investigaciones Médico Biológicas, Universidad Veracruzana, Veracruz, México.
H
H
Vivanco-Cid
Instituto de Investigaciones Médico Biológicas, Universidad Veracruzana, Veracruz, México.
I Y
IY
Izaguirre-Hernández
Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, IPN, México, DF, México.
I
I
Estrada-García
Unidad de Investigación Médica en Inmunoquímica, Hospital de Especialidades, Centro Médico Nacional "Siglo XXI", IMSS, México, DF, México.
L
L
Arriaga-Pizano
Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, IPN, México, DF, México.
R
R
Chacón-Salinas
Facultad de Estudios Superiores Cuautitlán, Universidad Nacional Autónoma de México, Cuatitlán-Izcalli, Estado de México, México.
S
S
Fonseca-Coronado
Departamento de Investigaciones Inmunológicas, Instituto de Diagnóstico y Referencia Epidemiológicos, Secretaría de Salud, México, DF, México.
G
G
Vaughan
Departamento de Investigaciones Inmunológicas, Instituto de Diagnóstico y Referencia Epidemiológicos, Secretaría de Salud, México, DF, México.
K Ruiz
KR
Tovar
Departamento de Investigaciones Inmunológicas, Instituto de Diagnóstico y Referencia Epidemiológicos, Secretaría de Salud, México, DF, México.
M P
MP
Rivera-Osorio
Departamento de Investigaciones Inmunológicas, Instituto de Diagnóstico y Referencia Epidemiológicos, Secretaría de Salud, México, DF, México. Electronic address: aescobargutierrez@yahoo.com.
A
A
Escobar-Gutiérrez
D000293:Adolescent; D000328:Adult; D002478:Cells, Cultured; D002648:Child; D003715:Dengue / Q000276:immunology*; D003716:Dengue Virus / Q000276:immunology*; D018450:Disease Progression; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007113:Immunity, Innate; D056747:Immunomodulation; D008297:Male; D008562:Membrane Glycoproteins / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology* / Q000821:virology; D009504:Neutrophils / Q000276:immunology* / Q000821:virology; D011971:Receptors, Immunologic / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D000073871:Triggering Receptor Expressed on Myeloid Cells-1; D055815:Young Adult
D008562:Membrane Glycoproteins; D011971:Receptors, Immunologic; C408842:TREM1 protein, human; D000073871:Triggering Receptor Expressed on Myeloid Cells-1
Dengue virus; Innate immunity; TREM-1; sTREM-1