title: Endotoxemia and endotoxin tolerance in patients with ARDS.
abstract: BACKGROUND
  The significance of endotoxemia in man is controversial, induces cytokine release and stimulates the immune system. Exaggerated cytokine release of mononuclear cells was observed in acute lung injury/acute respiratory distress syndrome (ALI/ARDS). However, repetitive administration of endotoxin can cause tolerance.
  
  
  OBJECTIVE
  To investigate endotoxemia, plasma TNFalpha, IL-1beta, IL-6, the liberation capacity of those cytokines from mononuclear cells after LPS challenge (Delta values), and plasma antibodies to endotoxins and alpha-hemolysin of Staphylococcus aureus in ALI/ARDS.
  
  
  METHODS
  A prospective clinical study was conducted.
  
  
  METHODS
  The study was carried out at the University Hospital Ulm, Ulm, Germany.
  
  
  METHODS
  The respondents were 23 patients with ALI/ARDS.
  
  
  METHODS
  ALI/ARDS was defined according to the American-European Consensus Conference on ARDS. Blood was collected periodically. Parameters were measured by LAL or ELISA.
  
  
  RESULTS
  ARDS (P(a)O(2)/F(i)O(2) < 200) revealed higher endotoxemia (0.22-0.46 [0.06-1.15] EU/mL vs 0.05-0.14 [0.02-0.63] EU/mL) than ALI (P(a)O(2)/F(i)O(2) > 200) but lower DeltaIL-6 (124-209 [10-1214] pg/mL vs 298-746 [5-1797] pg/mL), DeltaTNFalpha (50-100 [6-660] pg/mL vs 143-243 [12-2795] pg/mL), and DeltaIL-1 (2-3 [0-26] pg/mL vs 2-14 [0-99] pg/mL). Endotoxemia correlated negative with P(a)O(2)/F(i)O(2) (r, -0.44 to -0.50). All patients presented antibodies to lipopolysaccharides and alpha-hemolysin, but the level did not correlate with P(a)O(2)/F(i)O(2).
  
  
  CONCLUSIONS
  ALI/ARDS is associated with endotoxemia. The more severe the disease, the more intense is endotoxemia but the lower is the capacity of mononuclear cells to release cytokines (tolerance). Antibodies against Gram-positive and Gram-negative bacteria are detectable in the plasma but without relation to P(a)O(2)/F(i)O(2).
authors.affiliation: Department of General Surgery, University of Ulm, Ulm, Germany. klaus.buttenschoen@uniklinik-ulm.de
authors.forename: Klaus
authors.initials: K
authors.lastname: Buttenschoen
authors.forename: Marko
authors.initials: M
authors.lastname: Kornmann
authors.forename: Dieter
authors.initials: D
authors.lastname: Berger
authors.forename: Gerhard
authors.initials: G
authors.lastname: Leder
authors.forename: Hans G
authors.initials: HG
authors.lastname: Beger
authors.forename: Catalin
authors.initials: C
authors.lastname: Vasilescu
mesh_terms: D018806:APACHE; D055371:Acute Lung Injury / Q000276:immunology*; D000293:Adolescent; D000328:Adult; D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D001402:B-Lymphocytes / Q000276:immunology; D001427:Bacterial Toxins / Q000276:immunology; D019446:Endotoxemia / Q000276:immunology*; D004731:Endotoxins / Q000276:immunology; D005260:Female; D006460:Hemolysin Proteins / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology; D007136:Immunoglobulins; D053583:Interleukin-1beta / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood*; D008070:Lipopolysaccharides / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology; D010100:Oxygen / Q000097:blood; D011446:Prospective Studies; D012128:Respiratory Distress Syndrome / Q000276:immunology*; D013211:Staphylococcus aureus / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D055815:Young Adult
chemical_list: D000907:Antibodies, Bacterial; D001427:Bacterial Toxins; D004731:Endotoxins; D006460:Hemolysin Proteins; D007136:Immunoglobulins; D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; C042866:antilipopolysaccharide antibodies; C021091:staphylococcal alpha-toxin; D010100:Oxygen