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Infection and Immunity, December 2000, p. 6924-6931, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Interleukin-1 Receptor Type I Gene-Deficient Mice Are Less Susceptible to Staphylococcus epidermidis Biomaterial-Associated Infection than Are Wild-Type Mice

Jaap Jan Boelens,1,* Tom van der Poll,2 Sebastian A. J. Zaat,3 Jean L. A. N. Murk,3 Jan J. Weening,4 and Jacob Dankert3

Department of Pediatrics, Leiden University Medical Center, 2300 RC, Leiden,1 and Department of Medical Microbiology,3 Department of Experimental Internal Medicine,2 and Department of Pathology,4 Academic Medical Center, 1105 AZ, Amsterdam, The Netherlands

Received 8 March 2000/Returned for modification 24 April 2000/Accepted 24 August 2000

Elevated concentrations of interleukin-1 (IL-1) were found in tissue surrounding biomaterials infected with Staphylococcus epidermidis. To determine the role of IL-1 in biomaterial-associated infection (BAI), IL-1 receptor type I-deficient (IL-1R-/-) and wild-type mice received subcutaneous implants of silicon elastomer (SE) or polyvinylpyrrolidone-grafted SE (SEpvp), combined with an injection of 106 CFU of S. epidermidis or sterile saline. Neither mouse strain was susceptible to BAI around SE. IL-1R-/- mice with SEpvp implants had a no abscess formation and a reduced susceptibility to persistent S. epidermidis infection. The normal foreign body response, characterized by giant-cell formation and encapsulation, was delayed around SEpvp in wild-type mice but not in IL-1R-/- mice. This coincided with enhanced local IL-4 production in IL-1R-/- mice. These data suggest that inhibition of local IL-1 activity may be beneficial for the outcome of BAI.

* Corresponding author. Mailing address: Dept. of Pediatrics, P.O. Box 9600, J6-Q-208, 2300 RC Leiden, The Netherlands. Phone: 31 71 5262824. Fax: 31 71 5248198. E-mail: boelensjj{at}yahoo.com.

Infection and Immunity, December 2000, p. 6924-6931, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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