Nasal carriage of Staphylococcus aureus has been identified as a risk factor for community-acquired and nosocomial infections. We screened 230 donors of diverse ethnic and socioeconomic backgrounds and identified 62 (27%) whose nasal secretions were colonized by S. aureus. In 18 donors in whom the various regions of the nasal luminal surface were separately sampled, the predominant region of S. aureus colonization was the moist squamous epithelium on the septum adjacent to the nasal ostium. Nasal fluid from carriers was defective in killing endogenous S. aureus and nasal carrier isolates of S. aureus but not a laboratory S. aureus strain. Transmission electron microscopy revealed that S. aureus isolates incubated in nasal fluid from carriers for 2 h at 37°C were less damaged than those incubated in noncarrier fluid and were coated with an electron-dense layer. Compared with that from healthy donors and patients with acute rhinitis, nasal fluid from carriers contained elevated concentrations of the neutrophil-derived defensins human neutrophil peptides 1 to 3 (47-and 4-fold increases, respectively), indicative of a neutrophil-mediated inflammatory host response to S. aureus colonization. The concentration of the inducible epithelial antimicrobial peptide human ␤-defensin 2 was also highly elevated compared to that in healthy donors, in whom the level was below the detection limit, or patients with acute rhinitis (sixfold increase). Thus, nasal carriage of S. aureus takes hold in nasal fluid that is permissive for colonization and induces a local inflammatory response that fails to clear the colonizing bacteria.Nasal Staphylococcus aureus carriage, affecting about 20% of the population, has been identified as a risk factor for the pathogenesis of community-acquired and nosocomial infections (5, 12). The factors that determine carrier or noncarrier status are largely unknown. Various epithelial and mucous host factors, such as surface glycoproteins and proteoglycans, have been shown to mediate the binding of S. aureus, but the precise adhesive molecules on the host and bacteria have not been identified. S. aureus appears to attach to cell-associated and cell-free secretions (10) and to interact with receptor sites of secretory immunoglobulin A (1), glycolipids (6), and surfactant protein A (8). Various bacteria, including Staphylococcus epidermidis, are capable of reducing nasal ciliary activity in vitro (4). Enhanced adhesion and diminished mucociliary clearance could explain the retention of S. aureus within the nasal passageways but not its ability to grow to a high density in this normally nonpermissive environment.Recent studies have highlighted the innate antimicrobial properties of nasal fluid (2) and airway fluid in general (11). The current study explored the factors that contributed to S. aureus colonization in a cohort of donors with nasal S. aureus carriage. MATERIALS AND METHODSIdentifying carriers of S. aureus. Samples of nasal flora and nasal fluid were collected from healthy volunteer donors accordi...

CIMT is a good indicator of cardiovascular risk and provides a graded measure of vascular damage: no clear CIMT level above which the cardiovascular risk appears to increase considerably The evidence for arterial stiffness, assessed as carotid distensibility or aortic pulse wave velocity, as an indicator for risk of cardiovascular disease is restricted to subjects with either hypertension or end-stage renal disease or based on small studies in renal transplant patients and elderly. Evidence to indicate that information on carotid intima-media thickness or arterial stiffness, additional to established cardiovascular risk factors, helps to distinguish subjects into those with a high and those with a low absolute risk of cardiovascular disease is limited, but needed. Also, information on the direct comparison of both arterial stiffness measures in their ability to predict cardiovascular disease is needed.

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