Affiliation:
1. Departments of Medicine and Pathology and Will Rogers Institute for Pulmonary Research, UCLA School of Medicine, Los Angeles, California
Abstract
ABSTRACT
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 β-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.
Publisher
American Society for Microbiology
Subject
Microbiology (medical),Clinical Biochemistry,Immunology,Immunology and Allergy
Cited by
171 articles.
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