title: Host polymorphisms in interleukin 4, complement factor H, and C-reactive protein associated with nasal carriage of Staphylococcus aureus and occurrence of boils.
abstract: BACKGROUND
  Staphylococcus aureus is capable of persistently colonizing the vestibulum nasi. We hypothesized that polymorphisms in host inflammatory response genes and genetic variation in S. aureus contribute to susceptibility to S. aureus carriage and infection.
  
  
  METHODS
  The prevalence of persistent nasal carriage of S. aureus in 3851 participants aged 61-101 years was 18% (678 of 3851 participants), whereas 73% of volunteers (2804 of 3851) were not colonized. A total of 1270 individuals had boils. Polymorphisms in TNFA (C -863T), IL4 (C -542T), CFH (Tyr402His), and CRP (C1184T, C2042T, and C2911G) were determined. Genetic similarity among 428 S. aureus isolates was determined by use of amplified fragment length polymorphism analysis (AFLP)-mediated genotyping.
  
  
  RESULTS
  The IL4 -524 C/C host genotype was associated with an increased risk of persistent S. aureus carriage, irrespective of S. aureus AFLP genotype. The CRP haplotype 1184C; 2042C; 2911C was overrepresented in individuals who were not colonized . In individuals with boils, carriers of the CFH Tyr402 variant, and the CRP 2911 C/C genotype were overrepresented.
  
  
  CONCLUSIONS
  Persistent carriage of S. aureus is influenced by genetic variation in host inflammatory response genes. As would be expected in multifactorial host-microbe interactions, these effects are limited. Interestingly, host genotype was associated with the carriage of certain S. aureus genotypes. Apparently, a close interaction between host and bacterial determinants are prerequisites for long-term colonization.
authors.affiliation: Department of Pediatrics, Sophia Children's Hospital, University Medical Center, Rotterdam, The Netherlands.
authors.forename: Marieke
authors.initials: M
authors.lastname: Emonts
authors.forename: André G
authors.initials: AG
authors.lastname: Uitterlinden
authors.forename: Jan L
authors.initials: JL
authors.lastname: Nouwen
authors.forename: Isabella
authors.initials: I
authors.lastname: Kardys
authors.forename: Moniek P M de
authors.initials: MP
authors.lastname: Maat
authors.forename: Damian C
authors.initials: DC
authors.lastname: Melles
authors.forename: Jacqueline
authors.initials: J
authors.lastname: Witteman
authors.forename: Paulus T V M de
authors.initials: PT
authors.lastname: Jong
authors.forename: Henri A
authors.initials: HA
authors.lastname: Verbrugh
authors.forename: Albert
authors.initials: A
authors.lastname: Hofman
authors.forename: Peter W M
authors.initials: PW
authors.lastname: Hermans
authors.forename: Alex van
authors.initials: Av
authors.lastname: Belkum
mesh_terms: D002097:C-Reactive Protein / Q000235:genetics* / Q000378:metabolism; D002353:Carrier State; D015331:Cohort Studies; D017242:Complement Factor H / Q000235:genetics* / Q000378:metabolism; D004247:DNA / Q000235:genetics / Q000302:isolation & purification; D005667:Furunculosis / Q000453:epidemiology*; D006801:Humans; D015847:Interleukin-4 / Q000235:genetics* / Q000378:metabolism; D009666:Nose; D011110:Polymorphism, Genetic; D013203:Staphylococcal Infections / Q000453:epidemiology / Q000235:genetics / Q000382:microbiology; D013211:Staphylococcus aureus / Q000302:isolation & purification*
chemical_list: D015847:Interleukin-4; D017242:Complement Factor H; D002097:C-Reactive Protein; D004247:DNA