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Infection and Immunity, April 1999, p. 1640-1645, Vol. 67, No. 4
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Defensins Impair Phagocytic Killing by Neutrophils in Biomaterial-Related Infection

S. S. Kaplan,1,2,* R. P. Heine,3 and R. L. Simmons2

Departments of Pathology1 and Surgery,2 University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, and Department of Obstetrics, Gynecology, and Reproductive Sciences, Magee Women's Research Institute, Pittsburgh, Pennsylvania 152133

Received 21 September 1998/Returned for modification 2 November 1998/Accepted 5 January 1999

The implantation of foreign material carries a risk of infection which frequently is resistant to all treatment short of removing the implant. We have previously shown that these materials activate neutrophils by contact, leading to production of oxygen free radicals accompanied by release of granule products. Such activation further results in depletion of local host defenses, including the capacity of biomaterial-activated neutrophils to kill bacteria. Among the granule products released from neutrophils are small cationic antibacterial peptides (human neutrophil peptides [HNP]) known as defensins. Here we tested the hypothesis that defensins, released from activated neutrophils onto the surface of biomaterials, might play a role in the deactivation of subsequent neutrophil populations. Incubation of neutrophils with purified HNP resulted in a dose-related impairment of stimulus-induced oxygen radical production and of phagocytic killing. Furthermore, fresh neutrophils added to biomaterial-associated neutrophils exhibited impaired phagocytic killing. This impairment could be abrogated by antibody to HNP but not by an irrelevant antibody. Taken together, these observations support the idea that neutrophils activated at a material surface can create, by means of HNP release, an environment hostile to their microbicidal function and that of their infiltrating brethren.

* Corresponding author. Mailing address: University of Pittsburgh Medical Center, Room 5930 MT CHP, 200 Lothrop St., Pittsburgh, PA 15213. Phone: (412) 647-3772. Fax: (412) 647-8567. E-mail: kaplanss{at}msx.upmc.edu.

Infection and Immunity, April 1999, p. 1640-1645, Vol. 67, No. 4
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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