title: [Host inflammatory and anti-inflammatory response during sepsis].
abstract: Sepsis still remains the major complication for patients admitted in intensive care units (ICU), and is responsible for numerous deaths. ICU patients admitted after sepsis, hemorrhagic shock, severe trauma, severe burns or major surgery show a systemic inflammatory response syndrome (SIRS). This syndrome is characterized by an exacerbation of inflammation, with increased levels of pro- (IL-1β, TNFα, IL-6, IL-8) as well as anti-inflammatory (IL-10, IL-1Ra, TGFβ) cytokines into their bloodstream. During sepsis, the bacteria release microbial motifs such as peptidoglycan, lipopolysaccharide (LPS) and DNA that initiate the inflammatory response, and are involved in the onset of multiple organ failure. The same microbial motifs can also be found in patients with a SIRS of non-infectious origin, following the translocation of bacteria from their digestive tract. This translocation is certainly contributing to the difficulty of discriminating between septic and SIRS patients using biological markers. Furthermore, the host response is accompanied by an alteration of the ex vivo response of circulating leukocytes, particularly monocytes. This hyporesponsiveness to LPS is associated with a decreased activation of the transcription factor NF-κB (required for the expression of pro-inflammatory cytokines) and an increased expression of negative regulators of the NF-κB pathway. However, the leukocyte hyporesponsiveness is not a global phenomenon, it depends on the type of patient, on the receptor-activator pair, on the timing, and on the cytokine.
authors.affiliation: Unité cytokines et inflammation, département infection et épidémiologie, Institut Pasteur, 28, rue du Dr-Roux, 75015 Paris, France. minou.adib-conquy@pasteur.fr
authors.forename: M
authors.initials: M
authors.lastname: Adib-Conquy
authors.forename: J-M
authors.initials: JM
authors.lastname: Cavaillon
mesh_terms: D000893:Anti-Inflammatory Agents / Q000378:metabolism*; D054884:Host-Pathogen Interactions / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism*; D008954:Models, Biological; D018805:Sepsis / Q000276:immunology* / Q000378:metabolism; D015398:Signal Transduction / Q000276:immunology / Q000502:physiology; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology / Q000276:immunology / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators