title: The acute-phase response impairs host defence against Enterococcus faecium peritonitis.
abstract: Enterococcus faecium is an emerging pathogen that causes infections in hospitalized patients with various co-morbid diseases. These underlying diseases are often associated with an acute-phase response that renders patients vulnerable to nosocomial infections. To study the influence of the acute-phase response induced by sterile tissue injury on host defence against E. faecium, mice were injected subcutaneously with either turpentine or casein 1 day before intraperitoneal infection with E. faecium. Control mice were subcutaneously injected with saline or sodium bicarbonate, respectively. Turpentine and casein induced an acute-phase response as reflected by increases in the plasma concentrations of interleukin-6, serum amyloid P and C3. A pre-existent acute-phase response in mice was associated with a strongly reduced capacity to clear E. faecium, resulting in prolonged bacteraemia for several days. The inflammatory response to E. faecium was impaired in mice with an acute-phase response, as shown by reduced capacity to mount a neutrophilic leucocytosis in peripheral blood and by decreased local cytokine concentrations. These data indicate that the acute-phase response impairs host defence against E. faecium, suggesting that this condition may contribute to the increased vulnerability of critically ill patients to enterococcal infections.
authors.affiliation: Centre for Infection and Immunity Amsterdam (CINIMA), Amsterdam, the Netherlands. m.leendertse@amc.uva.nl
authors.forename: Masja
authors.initials: M
authors.lastname: Leendertse
authors.forename: Rob J L
authors.initials: RJ
authors.lastname: Willems
authors.forename: Ida A J
authors.initials: IA
authors.lastname: Giebelen
authors.forename: Petra S
authors.initials: PS
authors.lastname: van den Pangaart
authors.forename: Marc J M
authors.initials: MJ
authors.lastname: Bonten
authors.forename: Tom
authors.initials: T
authors.lastname: van der Poll
mesh_terms: D000210:Acute-Phase Reaction / Q000139:chemically induced / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D000818:Animals; D002364:Caseins / Q000494:pharmacology; D002614:Chelating Agents / Q000494:pharmacology; D003176:Complement C3 / Q000819:agonists / Q000276:immunology / Q000378:metabolism; D016207:Cytokines / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D016984:Enterococcus faecium / Q000187:drug effects / Q000276:immunology*; D005260:Female; D016908:Gram-Positive Bacterial Infections / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D015850:Interleukin-6 / Q000819:agonists / Q000097:blood; D007509:Irritants / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D010538:Peritonitis / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D000683:Serum Amyloid P-Component / Q000819:agonists / Q000276:immunology / Q000378:metabolism; D014425:Turpentine / Q000494:pharmacology
chemical_list: D002364:Caseins; D002614:Chelating Agents; D003176:Complement C3; D016207:Cytokines; D015850:Interleukin-6; D007509:Irritants; D000683:Serum Amyloid P-Component; D014425:Turpentine