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Infection and Immunity, June 2006, p. 3148-3155, Vol. 74, No. 6
0019-9567/06/$08.00+0     doi:10.1128/IAI.00087-06

Resistance of Streptococcus gordonii to Polymorphonuclear Leukocyte Killing Is a Potential Virulence Determinant of Infective Endocarditis

Si Young Lee,^1, John O. Cisar,^1* Joseph L. Bryant,^1, Michael A. Eckhaus,² and Ann L. Sandberg^1,

Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research,¹ Office of Research Services, Division of Veterinary Resources, National Institutes of Health, Bethesda, Maryland 20892²

Received 17 January 2006/ Returned for modification 24 February 2006/ Accepted 15 March 2006

Significant differences in virulence among seven representative Streptococcus gordonii strains were observed by using the rat model of infective endocarditis. Five strains, including S. gordonii DL1, caused severe disease, while the other two strains, including S. gordonii SK12, caused minimal or no disease. The differences in virulence were evident from the visible presence of streptococci in the vegetations present on the aortic valves of catheterized rats that were challenged with individual strains and also from the much greater recovery of rifampin-resistant S. gordonii DLl than of streptomycin-resistant S. gordonii SK12 from the hearts of animals coinfected with both organisms. Each S. gordonii strain aggregated with human platelets and bound to polymorphonuclear leukocytes (PMNs), as shown by the stimulation of PMN superoxide anion production. These interactions were reduced or abolished by pretreatment of the platelets or PMNs with sialidase, indicating that there was bacterial recognition of host sialic acid-containing receptors. Adhesin-mediated binding of each S. gordonii strain to PMNs also triggered phagocytosis. However, the subsequent PMN-dependent killing differed significantly for the seven strains. The five virulent strains included three strains that were not killed and two strains whose numbers were reduced by approximately 50%. In contrast, the level of killing of each avirulent strain under the same conditions was significantly greater and approached 90% of the bacteria added. Parallel studies performed with rat PMNs revealed comparable differences in the resistance or susceptibility of representative virulent and avirulent strains. Thus, the ability of S. gordonii to survive in PMNs following adhesin-mediated phagocytosis may be an important virulence determinant of infective endocarditis.

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* Corresponding author. Mailing address: Building 30, Room 3A-301, 30 Convent Drive, NIDCR, NIH, Bethesda, MD 20892-4352. Phone: (301) 496-1822. Fax: (301) 402-1064. E-mail: john.cisar{at}nih.gov.

Editor: J. N. Weiser

Present address: Department of Oral Microbiology, College of Dentistry, Research Institute of Oral Science, Kangnung National University, 210-702 Kangnung, Korea.

Present address: Institute of Human Virology, University of Maryland Biotechnology Institute, Baltimore, Md.

Present address: Building 45, Room 4AN-12, NIH, Bethesda, MD 20892.

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Infection and Immunity, June 2006, p. 3148-3155, Vol. 74, No. 6
0019-9567/06/$08.00+0     doi:10.1128/IAI.00087-06

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