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Infection and Immunity, February 2006, p. 947-952, Vol. 74, No. 2
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.2.947-952.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Interleukin 1{alpha} Increases the Susceptibility of Rabbits to Experimental Viridans Streptococcal Endocarditis

Jacob Dankert,1 Janneke van der Werff,2 Willem Joldersma,2 and Sebastian A. J. Zaat1*

Department of Medical Microbiology, Academic Medical Center, University of Amsterdam, Meibergdreef 15, 1105 AZ Amsterdam,1 Department of Hospital Epidemiology, University Medical Center Groningen, 9700 RB Groningen, The Netherlands2

Received 1 July 2005/ Returned for modification 21 September 2005/ Accepted 27 October 2005

Major predisposing conditions for infective endocarditis (IE) are the presence of a cardiac platelet-fibrin vegetation and of circulating bacteria with relatively low susceptibility to microbicidal activity of blood platelets. The influence of proinflammatory conditions on development of IE is unknown. We studied the effects of the presence of a catheter, inserted to induce platelet-fibrin vegetations, and of the proinflammatory cytokine interleukin-1{alpha} in rabbit experimental IE. Leaving the catheter in place after challenge with viridans streptococci predisposed for experimental IE. IE susceptibility rapidly decreased between 0 to 6 h after catheter removal. The catheter did not predispose for IE by providing a site for bacterial adherence, as almost all explanted catheters were culture negative. To mimic the proinflammatory influence of the catheter, rabbits were injected with interleukin-1{alpha} at 24 h after catheter removal and at 0, 1, and 3 h before bacterial challenge. Interleukin-1{alpha} injected 3 h prior to challenge significantly increased IE incidence due to a platelet releasate-susceptible Streptococcus oralis strain, with rapidly increasing numbers of bacteria within the vegetations. IE due to the Streptococcus sanguis strain less susceptible to platelet releasate was not enhanced. We conclude that proinflammatory stimuli, either a catheter or interleukin-1{alpha}, enhanced susceptibility to IE due to the platelet releasate-susceptible S. oralis. As with rabbits, temporary intravascular proinflammatory conditions may predispose for IE in humans at risk for this serious infection.

* Corresponding author. Mailing address: Department of Medical Microbiology, Academic Medical Center, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands. Phone: 31205664863. Fax: 31206979271. E-mail: S.A.Zaat{at}amc.uva.nl.

Editor: V. J. DiRita

Infection and Immunity, February 2006, p. 947-952, Vol. 74, No. 2
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.2.947-952.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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