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Infection and Immunity, July 1999, p. 3267-3275, Vol. 67, No. 7
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Innate Antimicrobial Activity of Nasal Secretions

Alexander M. Cole, Puneet Dewan, and Tomas Ganz*

Departments of Medicine and Pathology and the Will Rogers Institute for Pulmonary Research, UCLA School of Medicine, Los Angeles, California 90095

Received 9 February 1999/Returned for modification 19 March 1999/Accepted 2 April 1999

Minimally manipulated nasal secretions, an accessible form of airway surface fluid, were tested against indigenous and added bacteria by using CFU assays. Antimicrobial activity was found to vary between donors and with different target bacteria and was markedly diminished by dilution of the airway secretions. Donor-to-donor differences in electrophoresis patterns of nasal secretions in sodium dodecyl sulfate-polyacrylamide gel electrophoresis (PAGE) and acid urea-PAGE analyses were readily observed, suggesting that polymorphic genes encode the secreted proteins. Three donors (of twenty-four total), whose nasal fluid yielded similar protein band patterns and did not kill indigenous bacteria, were determined to be heavy nasal carriers of Staphylococcus aureus. Their fluid was deficient in microbicidal activity toward a colonizing strain of S. aureus but the defect was corrected in vitro by a 1:1 addition of nasal fluid from noncarriers. The microbicidal activity of normal fluid was inactivated by heating it for 10 min to 100°C and could not be restored solely by the addition of two major nasal antimicrobial proteins, lysozyme and lactoferrin. Several other known antimicrobial proteins and peptides, including statherin, secretory phospholipase A2, and defensins, were identified in nasal secretions and likely contribute to their total antimicrobial properties. Nasal fluid may serve as a useful model for the analysis of lower-airway secretions and their role in host defense against airway colonization and pulmonary infections.

* Corresponding author. Mailing address: Department of Medicine, Division of Pulmonary and Critical Care, UCLA School of Medicine, CHS 37-055, 10833 Le Conte Ave., Los Angeles, CA 90095-1690. Phone: (310) 825-7499. Fax: (310) 206-8766. E-mail: tganz{at}ucla.edu.

Infection and Immunity, July 1999, p. 3267-3275, Vol. 67, No. 7
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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