title: Bacterial DNA induces the complement system activation in serum and ascitic fluid from patients with advanced cirrhosis.
abstract: Translocation of intestinal bacteria to ascitic fluid is, probably, the first step in the development of spontaneous bacterial peritonitis in patients with cirrhosis. Proteins of the complement system are soluble mediators implicated in the host immune response to bacterial infections and its activation has been traditionally considered to be an endotoxin-induced phenomenon. The aim of this study was to compare the modulation of these proteins in response to the presence of bacterial DNA and/or endotoxin in patients with advanced cirrhosis and ascites in different clinical conditions. Groups I and II consisted of patients without/with bacterial DNA. Group III included patients with spontaneous bacterial peritonitis and Group IV with patients receiving norfloxacin as secondary long-term prophylaxis of spontaneous bacterial peritonitis. Serum and ascitic fluid levels of endotoxin and truncated residues of the complement system were measured by ELISA. The complement system is triggered in response to bacterial DNA, as evidenced by significantly increased levels of C3b, membrane attack complex, and C5a in patients from Groups II and III compared with patients without bacterial DNA (Group I) and those receiving norfloxacin (Group IV). Gram classification did not further differentiate the immune response between patients within groups II and III, even though endotoxin levels were, as expected, significantly higher in patients with bacterial DNA from gram-negative microorganisms. The complement protein activation observed in patients with bacterial DNA in blood and ascitic fluid is indistinguishable from that observed in patients with spontaneous bacterial peritonitis and may occur in an endotoxin-independent manner.
authors.affiliation: CIBERehd, Instituto de Salud Carlos III, Madrid, Spain.
authors.forename: Rubén
authors.initials: R
authors.lastname: Francés
authors.forename: José M
authors.initials: JM
authors.lastname: González-Navajas
authors.forename: Pedro
authors.initials: P
authors.lastname: Zapater
authors.forename: Carlos
authors.initials: C
authors.lastname: Muñoz
authors.forename: Rocío
authors.initials: R
authors.lastname: Caño
authors.forename: Sonia
authors.initials: S
authors.lastname: Pascual
authors.forename: Dorkas
authors.initials: D
authors.lastname: Márquez
authors.forename: Francia
authors.initials: F
authors.lastname: Santana
authors.forename: Miguel
authors.initials: M
authors.lastname: Pérez-Mateo
authors.forename: José
authors.initials: J
authors.lastname: Such
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D001201:Ascites / Q000150:complications / Q000276:immunology* / Q000382:microbiology; D001202:Ascitic Fluid / Q000737:chemistry / Q000276:immunology* / Q000382:microbiology; D001424:Bacterial Infections / Q000150:complications / Q000188:drug therapy / Q000276:immunology*; D018988:Bacterial Translocation / Q000276:immunology; D003167:Complement Activation / Q000187:drug effects / Q000276:immunology; D004269:DNA, Bacterial / Q000097:blood / Q000276:immunology* / Q000302:isolation & purification; D004731:Endotoxins / Q000097:blood / Q000276:immunology / Q000302:isolation & purification; D005260:Female; D006801:Humans; D008103:Liver Cirrhosis / Q000097:blood / Q000150:complications / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009643:Norfloxacin / Q000627:therapeutic use; D010538:Peritonitis / Q000150:complications / Q000188:drug therapy / Q000276:immunology*
chemical_list: D000900:Anti-Bacterial Agents; D004269:DNA, Bacterial; D004731:Endotoxins; D009643:Norfloxacin