title: The level of endotoxemia in sepsis varies in relation to the underlying infection: Impact on final outcome.
abstract: Former studies of our group have shown that the innate and adaptive immune status may differ in relation with the causative infection. To this same end, it was investigated if kinetics of circulating lipopolysaccharide (LPS) leading to inflammatory response may differ. Blood was sampled from 189 patients with sepsis and 206 with severe sepsis/shock starting 24h from advent of sepsis and repeating on day 3. Serum LPS was measured by Limulus Amebocyte Lysate (LAL) assay. From 59 patients, circulating monocytes were isolated and incubated in the absence/presence of LPS. Concentrations of tumor necrosis factor-alpha (TNFα) were measured in supernatants by an enzyme immunoassay. In either category of severity, circulating LPS was greater among sufferers from primary Gram-negative bacteremia (BSI) and from community-acquired pneumonia (CAP) than sufferers from other underlying infections. LPS were greater among patients with BSI compared to patients with secondary Gram-negative bacteremia and patients without bacteremia. Greater decrease of circulating LPS over 48h was recorded for survivors compared to non-survivors only within sufferers from BSI and CAP. Significant endotoxemia was considered for patients with serum LPS within the upper quartile of distribution; their monocytes were less potent for release of TNFα. It is concluded that endotoxemia in sepsis varies greatly with the underlying infection; this is related with immunoparalysis of monocytes with implications on final outcome.
authors.affiliation: Department of Surgery, Nafplion General Hospital, Greece.
authors.forename: Ioannis
authors.initials: I
authors.lastname: Kritselis
authors.forename: Vassiliki
authors.initials: V
authors.lastname: Tzanetakou
authors.forename: Georgios
authors.initials: G
authors.lastname: Adamis
authors.forename: George
authors.initials: G
authors.lastname: Anthopoulos
authors.forename: Eleni
authors.initials: E
authors.lastname: Antoniadou
authors.forename: Magdalini
authors.initials: M
authors.lastname: Bristianou
authors.forename: Anastasia
authors.initials: A
authors.lastname: Kotanidou
authors.forename: Michail
authors.initials: M
authors.lastname: Lignos
authors.forename: Kostantinos
authors.initials: K
authors.lastname: Polyzos
authors.forename: Theodoros
authors.initials: T
authors.lastname: Retsas
authors.forename: Panagiota
authors.initials: P
authors.lastname: Sassopoulou
authors.forename: Andrianna I
authors.initials: AI
authors.lastname: Papaioannou
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Sinapidis
authors.forename: Kalliopi
authors.initials: K
authors.lastname: Sereti
authors.forename: Vasileios
authors.initials: V
authors.lastname: Vittoros
authors.forename: Panagiotis
authors.initials: P
authors.lastname: Ghanas
authors.forename: Charalambos
authors.initials: C
authors.lastname: Gogos
authors.forename: Evangelos J
authors.initials: EJ
authors.lastname: Giamarellos-Bourboulis
mesh_terms: D000368:Aged; D019446:Endotoxemia / Q000276:immunology* / Q000401:mortality; D005260:Female; D016905:Gram-Negative Bacterial Infections / Q000097:blood* / Q000276:immunology*; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000276:immunology*; D008070:Lipopolysaccharides / Q000097:blood / Q000276:immunology; D008297:Male; D011014:Pneumonia / Q000097:blood / Q000276:immunology; D011446:Prospective Studies; D018805:Sepsis / Q000276:immunology* / Q000401:mortality; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha
keywords: Endotoxins; Monocytes; Outcome; Sepsis