The Role of Human Innate Immune Factors in Nasal Colonization by Staphylococcus Aureus

Microbes Infect. 2007 Oct;9(12-13):1471-7. doi: 10.1016/j.micinf.2007.08.003. Epub 2007 Aug 10.


Staphylococcus aureus colonization of the human nares predisposes to sometimes severe auto-infection. To investigate whether genetic polymorphism affects the S. aureus carriage status, sequence variation in alpha-defensin and beta-defensin, and mannose-binding lectin (MBL) genes were determined for a group of volunteers (n=109) with known S. aureus nasal carriage status. DEFA1/3 expression was measured in a subset of the volunteers (n=32). None of the single nucleotide polymorphisms studied could clearly distinguish the (non) carriage groups. S. aureus carriers differed from non-carriers in baseline level of HNP1-3 peptide production (median: 218 versus 89mug/ml, P=0.016). No association between HNP1-3 levels and the individual sequence polymorphisms was documented. The combined copy numbers of DEFA1/A3 genes ranged from 5 to 23 per diploid genome. A linear correlation between combined copy numbers and HNP1-3 peptide concentrations in nasal secretions of non-carriers was noted (r(2)=0.8991). DEFA3 gene was absent in 25% of the individuals. MBL haplotype A was overrepresented in persistent S. aureus carriers (87% vs. 67%; P=0.038). In conclusion, defensin gene polymorphism, both in sequence and in gene copy numbers, does not seem to be involved in S. aureus carriage predisposition. However, MBL haplotypes do so significantly. Baseline HNP1-3 production is more the consequence of S. aureus colonization than a reason for the (non) carrier status.

MeSH terms

  • Carrier State / microbiology*
  • Gene Dosage
  • Humans
  • Immunity, Innate
  • Mannose-Binding Lectin / genetics*
  • Mannose-Binding Lectin / metabolism
  • Nasal Cavity / immunology
  • Nasal Cavity / microbiology*
  • Polymerase Chain Reaction
  • Polymorphism, Genetic
  • Polymorphism, Restriction Fragment Length
  • Polymorphism, Single Nucleotide*
  • Staphylococcus aureus / growth & development*
  • alpha-Defensins / genetics*
  • alpha-Defensins / metabolism
  • beta-Defensins / genetics*
  • beta-Defensins / metabolism


  • Mannose-Binding Lectin
  • alpha-Defensins
  • beta-Defensins
  • human neutrophil peptide 1