title: Decreased plasma concentrations of apolipoprotein M in sepsis and systemic inflammatory response syndromes.
abstract: BACKGROUND
  Apolipoprotein M (apoM) is present in 5% of high-density lipoprotein (HDL) particles in plasma. It is a carrier of sphingosine-1-phosphate (S1P), which is important for vascular barrier protection. The aim was to determine the plasma concentrations of apoM during sepsis and systemic inflammatory response syndrome (SIRS) and correlate them to levels of apolipoprotein A-I (apoA1), apolipoprotein B (apoB), HDL-, and low-density lipoprotein (LDL)-cholesterol.
  
  
  METHODS
  Plasma samples from patients with (1), severe sepsis with shock (n = 26); (2), severe sepsis without shock (n = 44); (3), sepsis (n = 100); (4), infections without SIRS (n = 43); and (5) SIRS without infection (n = 20) were analyzed. The concentrations of apoM, apoA1, and apoB were measured with enzyme-linked immunosorbent assays (ELISAs). Total, HDL-, and LDL-cholesterol concentrations were measured with a commercial HDL/LDL cholesterol test.
  
  
  RESULTS
  ApoM concentrations correlated negatively to acute-phase markers. Thus, apoM behaved as a negative acute-phase protein. Decreased values were observed in all patient groups (P < 0.0001), with the most drastic decreases observed in the severely sick patients. ApoM levels correlated strongly to those of apoA1, apoB, HDL, and LDL cholesterol. The HDL and LDL cholesterol levels were low in all patient groups, as compared with controls (P < 0.0001), in particular, HDL cholesterol. ApoA1 and apoB concentrations were low only in the more severely affected patients.
  
  
  CONCLUSIONS
  During sepsis and SIRS, the plasma concentrations of apoM decrease dramatically, the degree of decrease reflecting the severity of the disease. As a carrier for barrier-protective S1P in HDL, the decrease in apoM could contribute to the increased vascular leakage observed in sepsis and SIRS.
authors.affiliation: Department of Laboratory Medicine, Division of Clinical Chemistry, Lund University, Skåne University Hospital, Entrance 46, Malmö, SE-20502, Sweden.
authors.forename: Sunil B
authors.initials: SB
authors.lastname: Kumaraswamy
authors.forename: Adam
authors.initials: A
authors.lastname: Linder
authors.forename: Per
authors.initials: P
authors.lastname: Åkesson
authors.forename: Björn
authors.initials: B
authors.lastname: Dahlbäck
mesh_terms: D000328:Adult; D001053:Apolipoproteins / Q000097:blood*; D001055:Apolipoproteins B / Q000097:blood; D000075243:Apolipoproteins M; D016022:Case-Control Studies; D008078:Cholesterol, LDL / Q000097:blood; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D054834:Lipocalins / Q000097:blood*; D008075:Lipoproteins, HDL / Q000097:blood; D008297:Male; D011446:Prospective Studies; D018805:Sepsis / Q000097:blood*; D018709:Statistics, Nonparametric; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood*
chemical_list: C400523:APOM protein, human; D001053:Apolipoproteins; D001055:Apolipoproteins B; D000075243:Apolipoproteins M; D008078:Cholesterol, LDL; D054834:Lipocalins; D008075:Lipoproteins, HDL