The role of human innate immune factors in nasal colonization by Staphylococcus aureus.

Journal article

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.

Authors: van Belkum, A; Emonts, M; Wertheim, H; de Jongh, C; Nouwen, J

• Publication status: Published
• Journal: Microbes and infection / Institut Pasteur
• Volume: 9
• Issue: 12-13
• Pages: 1471-1477
• Publication date: 2007-10-01
• DOI: 10.1016/j.micinf.2007.08.003
• EISSN: 1769-714X
• ISSN: 1286-4579
• Language: English
• Keywords: Immunity, Innate; Humans; Staphylococcus aureus; Mannose-Binding Lectin; Polymerase Chain Reaction; beta-Defensins; Gene Dosage; Polymorphism, Genetic; alpha-Defensins; Carrier State; Polymorphism, Single Nucleotide; Nasal Cavity; Polymorphism, Restriction Fragment Length