title: Up regulation of C3, C4, and soluble intercellular adhesion molecule-1 co-expresses with high sensitivity C reactive protein in familial hypoalphalipoproteinaemia: further evidence of inflammatory activation.
abstract: OBJECTIVE
  To test the working hypothesis that inflammation underlying precocious and severe coronary atherosclerotic disease in familial hypoalphalipoproteinaemia (FH) can be mediated by up regulation of the innate immune response.
  
  
  RESULTS
  52 patients with FH were compared with 52 healthy controls with regard to immune system markers such as C reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), C3c, and C4. Patients differed from controls in their significantly lower concentrations of high density lipoprotein cholesterol (30.2 (4.0) v 50.5 (13.6) mg/dl, p < 0.0001) and apolipoprotein A I (113.2 (19.9) v 148.7 (25.1) mg/dl, p < 0.0001) and their higher triglyceride (139.3 (63.2) v 81.4 (41.7) mg/dl, p < 0.0001) and CRP plasma concentrations (median 0.33 mg/dl, range 0.02-4.66 mg/dl v median 0.07 mg/dl, range 0.02-0.85 mg/dl, p < 0.0001), but not in their total cholesterol and low density lipoprotein cholesterol concentrations. Concentrations of protein complement were higher in patients (C3: 150.8 (42.3) v 101.9 (17.4) mg/dl, p < 0.0001; C4: 35.5 (13.6) v 22.8 (6.4) mg/dl, p < 0.0001) and sICAM-1 concentrations were more than double those found in the controls (335.1 (107.5) v 159.5 (78.2) mg/dl, p < 0.0001).
  
  
  CONCLUSIONS
  Increased concentrations of sICAM-1, C3c, and C4 co-express with high concentrations of CRP in FH. The lack of signs and symptoms of inflammation in these patients may suggest that the immune response is up regulated as part of the pro-inflammatory mechanisms that are activated in this atherogenic condition.
authors.affiliation: CNR Institute of Clinical Physiology, University of Pisa, Via Moruzzi, 1-56010 Pisa, Italy. tizisamp@ifc.cnr.it
authors.forename: T
authors.initials: T
authors.lastname: Sampietro
authors.forename: F
authors.initials: F
authors.lastname: Bigazzi
authors.forename: B
authors.initials: B
authors.lastname: Dal Pino
authors.forename: G
authors.initials: G
authors.lastname: Rossi
authors.forename: E
authors.initials: E
authors.lastname: Chella
authors.forename: S
authors.initials: S
authors.lastname: Lusso
authors.forename: M
authors.initials: M
authors.lastname: Puntoni
authors.forename: M
authors.initials: M
authors.lastname: Tuoni
authors.forename: A
authors.initials: A
authors.lastname: Bionda
mesh_terms: D016632:Apolipoprotein A-I / Q000097:blood; D002097:C-Reactive Protein; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003176:Complement C3 / Q000032:analysis / Q000378:metabolism*; D015932:Complement C3c / Q000378:metabolism; D003181:Complement C4 / Q000032:analysis / Q000378:metabolism*; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D013631:Tangier Disease / Q000097:blood / Q000378:metabolism*; D014280:Triglycerides / Q000097:blood; D015854:Up-Regulation / Q000502:physiology
chemical_list: D016632:Apolipoprotein A-I; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D003176:Complement C3; D003181:Complement C4; D014280:Triglycerides; D018799:Intercellular Adhesion Molecule-1; D015932:Complement C3c; D002097:C-Reactive Protein