title: Low immunogenicity allows Staphylococcus epidermidis to cause PD peritonitis.
abstract: BACKGROUND
  Peritonitis is a common and serious complication of peritoneal dialysis (PD). Coagulase-negative staphylococci from the patient's own skin flora are the most commonly found micro-organisms.
  
  
  OBJECTIVE
  In the present study we aim to elucidate the immune response in the early stage of infection and to clarify the importance of bacterial attachment to fibrinogen.
  
  
  METHODS
  Clinical Staphylococcus epidermidis isolates collected from PD peritonitis or the residential skin flora of healthy individuals were used to infect monocytes, macrophages, and peripheral blood mononuclear cells (PBMC) in the presence or absence of fibrinogen. The S. epidermidis strain HB (fbe(+)), expressing the fibrinogen-binding protein Fbe, and its isogenic mutant ST056 (fbe(-)) were used to study the impact of Fbe during cell infection. Immune induction was measured as interleukin-8 (IL-8) production determined by ELISA. Modulation of CD11b/CD18 expression in neutrophils incubated in conditioned medium from these experiments was analyzed in order to judge the cellular response.
  
  
  RESULTS
  S. epidermidis causing peritonitis was less immunogenic compared to strains belonging to the residential skin flora, as measured by IL-8 induction in monocytes and CD11b/CD18 expression in neutrophils. At low bacterial concentrations, attachment to fibrinogen was a prerequisite for an IL-8 induction in monocytes and PBMC. The fibrinogen-binding protein Fbe did not, however, influence immune induction under this condition.
  
  
  CONCLUSIONS
  We suggest that S. epidermidis strains may be able to cause clinical infection by evoking an inadequate immunological response in the early stage of infection. Bacterial attachment to fibrinogen is a relevant event during this phase but independent of the fibrinogen-binding protein Fbe.
authors.affiliation: Clinical Microbiology, Karolinska University Hospital and Karolinska Institutet, Stockholm, Sweden.
authors.forename: Karin
authors.initials: K
authors.lastname: Jung
authors.forename: Petra
authors.initials: P
authors.lastname: Lüthje
authors.forename: Joachim
authors.initials: J
authors.lastname: Lundahl
authors.forename: Annelie
authors.initials: A
authors.lastname: Brauner
mesh_terms: D002460:Cell Line; D004797:Enzyme-Linked Immunosorbent Assay; D005434:Flow Cytometry; D005500:Follow-Up Studies; D006801:Humans; D007111:Immunity, Cellular; D016209:Interleukin-8 / Q000096:biosynthesis; D017737:Macrophages, Peritoneal / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D010530:Peritoneal Dialysis / Q000009:adverse effects*; D010538:Peritonitis / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D013203:Staphylococcal Infections / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D013212:Staphylococcus epidermidis / Q000302:isolation & purification*
chemical_list: D016209:Interleukin-8