title: Mannose-binding lectin (MBL2) and ficolin-2 (FCN2) polymorphisms in patients on peritoneal dialysis with staphylococcal peritonitis.
abstract: BACKGROUND
  Mannose-binding lectin (MBL) and ficolin-2 (FCN) are activators of the lectin pathway of complement and act as primary defences against infection. Single-nucleotide polymorphisms (SNPs) in the MBL2 and FCN2 genes influence the functionality of the proteins. Both proteins are capable of binding staphylococci, which are pathogens that frequently cause peritonitis in patients on continuous ambulatory peritoneal dialysis (CAPD). We studied the role of polymorphisms in the MBL2 and FCN2 genes as a risk factor for developing CAPD peritonitis caused by staphylococci.
  
  
  METHODS
  We analysed SNPs in the MBL2 and FCN2 genes in 40 CAPD patients with staphylococcal peritonitis and in 65 CAPD patients without any history of peritonitis. Additionally, we analysed the prevalence of exit site infections and nasal Staphylococcus aureus carriage in both groups.
  
  
  RESULTS
  The + 6359C > T SNP leading to the Thr236Met amino acid alteration in the FCN2 gene, associated with decreased substrate binding, was significantly more prevalent in CAPD patients with a history of staphylococcal peritonitis compared with patients on CAPD without a history of peritonitis (P = 0.037). No difference was found in MBL2 genotypes between the two groups. In CAPD patients with a history of staphylococcal peritonitis, exit site infection with S. aureus was also more prevalent (P < 0.01), while S. aureus carriage was not (P = 0.073).
  
  
  CONCLUSIONS
  In addition to known risk factors such as exit site infection, the + 6359C > T SNP in the FCN2 gene might be a risk factor for staphylococcal peritonitis in CAPD patients due to decreased binding of FCN to staphylococci.
authors.affiliation: Department of Internal Medicine, St Antonius Hospital, Nieuwegein, The Netherlands. s.meijvis@antonius.net
authors.forename: Sabine C A
authors.initials: SC
authors.lastname: Meijvis
authors.forename: Bjorn L
authors.initials: BL
authors.lastname: Herpers
authors.forename: Henrik
authors.initials: H
authors.lastname: Endeman
authors.forename: Ben
authors.initials: B
authors.lastname: de Jong
authors.forename: Erik
authors.initials: E
authors.lastname: van Hannen
authors.forename: Heleen
authors.initials: H
authors.lastname: van Velzen-Blad
authors.forename: Raymond T
authors.initials: RT
authors.lastname: Krediet
authors.forename: Dirk G
authors.initials: DG
authors.lastname: Struijk
authors.forename: Douwe H
authors.initials: DH
authors.lastname: Biesma
authors.forename: Willem Jan W
authors.initials: WJ
authors.lastname: Bos
mesh_terms: D016022:Case-Control Studies; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D005919:Glomerular Filtration Rate; D006801:Humans; D037102:Lectins / Q000235:genetics*; D008297:Male; D037601:Mannose-Binding Lectin / Q000235:genetics*; D008875:Middle Aged; D010531:Peritoneal Dialysis, Continuous Ambulatory / Q000009:adverse effects*; D010538:Peritonitis / Q000209:etiology*; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D011379:Prognosis; D012189:Retrospective Studies; D012307:Risk Factors; D013203:Staphylococcal Infections / Q000209:etiology*; D013211:Staphylococcus aureus / Q000235:genetics / Q000472:pathogenicity; D015996:Survival Rate; D000097604:Ficolins
chemical_list: D037102:Lectins; D037601:Mannose-Binding Lectin; D000097604:Ficolins; C445619:MBL2 protein, human