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

Slaphylococcus 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. DEFA113 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 HNP 1 - 3 peptide production (median: 218 versus 89 mu g/ml, P = 0.016). No association between HNPI-3 levels and the individual sequence polymorphisms was documented. The combined copy numbers of DEFAIIA3 genes ranged from 5 to 23 per diploid genome. A linear correlation between combined copy numbers and HNPI-3 peptide concentrations in nasal secretions of non-carriers was noted (r(2) = 0.8991). DEFA3 gene was absent in 25% of the individuals. MEL 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 HNPI - 3 production is more the consequence of S. aureus colonization than a reason for the (non) carrier status. (c) 2007 Elsevier Masson SAS. All rights reserved.