title: Does soluble triggering receptor expressed on myeloid cells-1 play any role in the pathogenesis of septic shock?
abstract: In order to define the significance of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) upon progression from sepsis or severe sepsis to septic shock a prospective study was designed with 90 enrolled patients with septic syndrome due to ventilator-associated pneumonia. Blood was sampled on seven consecutive days upon initiation of symptoms and concentrations of tumour necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6), IL-8 and sTREM-1 were estimated in serum by an enzymeimmunoassay. No differences in concentrations of TNFalpha, IL-6 and IL-8 were found between patients with sepsis, severe sepsis and septic shock on the first day of presentation of symptoms. Patients presenting with septic shock had concentrations of sTREM-1 significantly higher than both patients with sepsis and severe sepsis on the first day; no difference was found between patients with sepsis and severe sepsis. A positive correlation was detected between sTREM-1 and the white blood cell count. Serum levels of sTREM-1 were significantly lower in patients where VAP resolved compared to those where VAP did not resolve; similar findings were noted between patients who eventually survived and those who died. IL-6 followed the kinetics of sTREM-1 in correlation to patients's prognosis; levels of TNFalpha and IL-8 were unrelated to prognosis. It is concluded that sTREM-1 is particularly increased upon evolution from sepsis or severe sepsis to septic shock. Its sustained increase is an indication of poor outcome. The underlined pathophysiological role of sTREM-1 for the transition from sepsis or severe sepsis to septic shock might constitute a novel target for immunomodulatory therapy.
authors.affiliation: 1st Department of Critical Care, University of Athens Medical School, Greece.
authors.forename: C
authors.initials: C
authors.lastname: Routsi
authors.forename: E J
authors.initials: EJ
authors.lastname: Giamarellos-Bourboulis
authors.forename: A
authors.initials: A
authors.lastname: Antonopoulou
authors.forename: S
authors.initials: S
authors.lastname: Kollias
authors.forename: S
authors.initials: S
authors.lastname: Siasiakou
authors.forename: A
authors.initials: A
authors.lastname: Koronaios
authors.forename: S
authors.initials: S
authors.lastname: Zakynthinos
authors.forename: A
authors.initials: A
authors.lastname: Armaganidis
authors.forename: H
authors.initials: H
authors.lastname: Giamarellou
authors.forename: C
authors.initials: C
authors.lastname: Roussos
mesh_terms: D000368:Aged; D018450:Disease Progression; D005260:Female; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D008562:Membrane Glycoproteins / Q000276:immunology*; D008875:Middle Aged; D011014:Pneumonia / Q000276:immunology; D011446:Prospective Studies; D011971:Receptors, Immunologic / Q000276:immunology*; D018805:Sepsis / Q000097:blood / Q000276:immunology; D012772:Shock, Septic / Q000097:blood / Q000276:immunology*; D000073871:Triggering Receptor Expressed on Myeloid Cells-1; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D015850:Interleukin-6; D016209:Interleukin-8; D008562:Membrane Glycoproteins; D011971:Receptors, Immunologic; C408842:TREM1 protein, human; D000073871:Triggering Receptor Expressed on Myeloid Cells-1; D014409:Tumor Necrosis Factor-alpha