title: Serum lipopolysaccharide-binding protein in endotoxemic patients with inflammatory bowel disease.
abstract: BACKGROUND
  In inflammatory bowel disease (IBD), enhanced inflammatory activity in the gut is thought to increase the risk of bacterial translocation and endotoxemia. By searching for signs of endotoxin-signaling cascade activation, including augmented levels of endotoxin, lipopolysaccharide-binding protein (LBP), and soluble CD14 receptor (sCD14), this prospective study sought to establish whether endotoxemia could contribute to greater clinical activity of disease.
  
  
  METHODS
  Concentrations of plasma endotoxin, LBP, sCD14, several cytokines, acute phase proteins and clinical activity indices were determined in 104 patients with Crohn's disease (CD) and 52 patients with ulcerative colitis (UC).
  
  
  RESULTS
  Endotoxemia was present in 48% of the patients with CD and in 28% of the patients with UC. The mean LBP was higher in patients with active CD (23.1 +/- 13.7 microg/mL) and UC (21.4 +/- 10.9 microg/mL) than in healthy controls (7.2 +/- 1.8 microg/mL; P < 0.01). Elevated serum concentrations of endotoxin and LBP were even detected in patients with inactive CD. Among the patients with active IBD, those with higher endotoxin levels had the worst clinical activity scores and the highest LBP levels. Treatment normalized LBP concentrations, from 29.1 +/- 13.0 to 15.2 +/- 7.3 microg/mL; (P < 0.05) in active CD and from 21.7 +/- 9.8 to 13.6 +/- 5.7 microg/mL; (P < 0.01) in active UC, along with normalizing endotoxin and sCD14 plasma concentrations.
  
  
  CONCLUSIONS
  Patients with IBD show increased serum levels of endotoxin, LBP and sCD14. This alteration correlates with disease activity, with normal levels recovered after treatment, although less completely in Crohn's disease, and parallels a rise in proinflammatory cytokines, suggesting a contribution of bacterial products to the inflammatory cascade in these patients.
authors.affiliation: Servicio de Bioquímica Clínica, Hospital Universitario Ramón y Cajal, Madrid, Spain.
authors.forename: Oscar
authors.initials: O
authors.lastname: Pastor Rojo
authors.forename: Antonio
authors.initials: A
authors.lastname: López San Román
authors.forename: Eduardo
authors.initials: E
authors.lastname: Albéniz Arbizu
authors.forename: Antonio
authors.initials: A
authors.lastname: de la Hera Martínez
authors.forename: Eduardo
authors.initials: E
authors.lastname: Ripoll Sevillano
authors.forename: Agustín
authors.initials: A
authors.lastname: Albillos Martínez
mesh_terms: D000209:Acute-Phase Proteins; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D018988:Bacterial Translocation; D015415:Biomarkers / Q000097:blood; D002352:Carrier Proteins / Q000097:blood*; D016022:Case-Control Studies; D003093:Colitis, Ulcerative / Q000097:blood / Q000382:microbiology*; D003424:Crohn Disease / Q000097:blood / Q000382:microbiology*; D019446:Endotoxemia / Q000097:blood* / Q000150:complications; D004731:Endotoxins / Q000097:blood; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D018950:Lipopolysaccharide Receptors / Q000097:blood; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood*; D008875:Middle Aged; D011446:Prospective Studies; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D015415:Biomarkers; D002352:Carrier Proteins; D004731:Endotoxins; D018836:Inflammation Mediators; D018950:Lipopolysaccharide Receptors; D008562:Membrane Glycoproteins; D000099231:Lipopolysaccharide-Binding Protein