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Infection and Immunity, February 2000, p. 644-650, Vol. 68, No. 2
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Role of Serotype-Specific Polysaccharide in the Resistance of Streptococcus mutans to Phagocytosis by Human Polymorphonuclear Leukocytes

Hiromasa Tsuda,1 Yoshihisa Yamashita,1 Kuniaki Toyoshima,2 Noboru Yamaguchi,1 Takahiko Oho,1 Yoshio Nakano,1 Kengo Nagata,3 and Toshihiko Koga1,*

Departments of Preventive Dentistry1 and Oral Anatomy,3 Kyushu University Faculty of Dentistry, Fukuoka 812-8582, and Department of Oral Anatomy II, Kyushu Dental College, Kitakyushu 803-8580,2 Japan

Received 17 May 1999/Returned for modification 1 July 1999/Accepted 15 November 1999

To clarify the role of cell surface components of Streptococcus mutans in resistance to phagocytosis by human polymorphonuclear leukocytes (PMNs), several isogenic mutants of S. mutans defective in cell surface components were studied with a luminol-enhanced chemiluminescence (CL) assay, a killing assay, and a transmission electron microscope. The CL responses of human PMNs to mutant Xc11 defective in a major cell surface antigen, PAc, and mutant Xc16 defective in two surface glucosyltransferases (GTF-I and GTF-SI) were the same as the response to the wild-type strain, Xc. In contrast, mutant Xc24R, which was defective in serotype c-specific polysaccharide, induced a markedly higher CL response than the other strains. The killing assay showed that human PMNs killed more Xc24R than the parent strain and the other mutants. The transmission electron microscopic observation indicated that Xc24R cells were more internalized by human PMNs than the parental strain Xc. These results may be reflected by the fact that strain Xc24R was more phagocytosed than strain Xc. The CL response of human PMNs to a mutant defective in polysaccharide serotype e or f was similar to the response to Xc24R. Furthermore, mutants defective in serotype-specific polysaccharide were markedly more hydrophobic than the wild-type strains and the other mutants, suggesting that the hydrophilic nature of polysaccharides may protect the bacterium from phagocytosis. We conclude that the serotype-specific polysaccharide, but not the cell surface proteins on the cell surface of S. mutans, may play an important role in the resistance to phagocytosis.

* Corresponding author. Mailing address: Department of Preventive Dentistry, Kyushu University Faculty of Dentistry, Fukuoka 812-8582, Japan. Phone: (92) 642-6350. Fax: (92) 642-6354. E-mail: toshidha{at}mbox.nc.kyushu-u.ac.jp.

Infection and Immunity, February 2000, p. 644-650, Vol. 68, No. 2
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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