title: Differential pattern of cell-surface and soluble TREM-1 between sepsis and SIRS.
abstract: OBJECTIVE
  Triggering receptor expressed on myeloid cells-1 (TREM-1) was reported to play a key roll in amplification of production of inflammatory cytokines. TREM-1 is suggested to be a specific biomarker for sepsis for this reason, but the clinical significance of TREM-1 has not been elucidated. We investigated TREM-1 expression on the cell-surface, and plasma levels of soluble TREM-1 (sTREM-1) in patients with non-infectious systemic inflammatory response syndrome (SIRS) and sepsis admitted to the ICU.
  
  
  METHODS
  Thirty-five patients with SIRS and 21 patients with sepsis admitted to ICU were subjected to the study. TREM-1 expressions on the surfaces of monocytes and neutrophils were measured by flow cytometry. Plasma sTREM-1 level and serum interleukin (IL)-6 level were measured.
  
  
  RESULTS
  Septic patients had decreased TREM-1 expression, clearly on neutrophils or to a lesser extent on monocyte compared to SIRS patients on ICU admission (neutrophils p<0.001, monocyte p<0.05). TREM-1 expression on neutrophils had a significant inverse correlation with serum IL-6 level (r=-0.64, p<0.0001). Plasma sTREM-1 level in septic patients was significantly higher than that in SIRS patients (p<0.05). Plasma sTREM-1 level positively correlated with severity score and non-survivors had increased plasma sTREM-1 level compared to survivors in all SIRS/sepsis patients (p<0.05).
  
  
  CONCLUSIONS
  Patients with sepsis had increased soluble TREM-1 and decreased TREM-1 expression on neutrophil compared to SIRS patients. sTREM-1 may be useful to evaluate disease severity and outcome of patients with SIRS or sepsis.
authors.affiliation: Department of Emergency and Critical Care Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan. okurere000@gmail.com
authors.forename: Reiko
authors.initials: R
authors.lastname: Oku
authors.forename: Shigeto
authors.initials: S
authors.lastname: Oda
authors.forename: Taka-aki
authors.initials: TA
authors.lastname: Nakada
authors.forename: Tomohito
authors.initials: T
authors.lastname: Sadahiro
authors.forename: Masataka
authors.initials: M
authors.lastname: Nakamura
authors.forename: Yoh
authors.initials: Y
authors.lastname: Hirayama
authors.forename: Ryuzo
authors.initials: R
authors.lastname: Abe
authors.forename: Yoshihisa
authors.initials: Y
authors.lastname: Tateishi
authors.forename: Michihiro
authors.initials: M
authors.lastname: Ito
authors.forename: Toru
authors.initials: T
authors.lastname: Iseki
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Hirasawa
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D016207:Cytokines / Q000096:biosynthesis; D005260:Female; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood / Q000378:metabolism*; D008565:Membrane Proteins / Q000096:biosynthesis / Q000378:metabolism; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism*; D009504:Neutrophils / Q000378:metabolism*; D011971:Receptors, Immunologic / Q000097:blood / Q000378:metabolism*; D018805:Sepsis / Q000097:blood / Q000378:metabolism*; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000378:metabolism*; D000073871:Triggering Receptor Expressed on Myeloid Cells-1
chemical_list: D015415:Biomarkers; D016207:Cytokines; D015850:Interleukin-6; D008562:Membrane Glycoproteins; D008565:Membrane Proteins; D011971:Receptors, Immunologic; C408842:TREM1 protein, human; D000073871:Triggering Receptor Expressed on Myeloid Cells-1