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Infection and Immunity, December 2000, p. 6785-6789, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Cytokine Induction by Streptococcus mutans and Pulpal Pathogenesis

Chin-Lo Hahn,1,2,* Al M. Best,2,3 and John G. Tew2

Department of Endodontics,1 Department of Biostatistics,3 and Clinical Research Center for Periodontal Diseases,2 School of Dentistry, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, Virginia 23298

Received 18 July 2000/Returned for modification 17 August 2000/Accepted 6 September 2000

Chronic pulpal inflammation under caries appears to be elicited by bacterial antigens that diffuse into the pulp through dentinal tubules. This prompted the hypothesis that cytokines elicited by antigens from Streptococcus mutans, which frequently dominates shallow lesions, could play a major role in eliciting the initial T-cell response in the pulp. To test this, we examined the ability of S. mutans to stimulate T cells and elicit cytokines and used Lactobacillus casei, which often predominates in deep carious lesions where B cells and plasma cells predominate, as a control. In addition, the presence of cytokines in the pulp was analyzed at the mRNA level. S. mutans elicited potent gamma interferon (IFN-gamma ) responses in peripheral blood mononuclear cell cultures and reduced the CD4/CD8 ratio by promoting CD8+ T cells. Multiple inflammatory cytokine mRNAs (IFN-gamma , interleukin 4 [IL-4], and IL-10) were detected in human dental pulp. A higher prevalence of IFN-gamma (67%) than IL-4 (19%) or IL-10 (29%) was obtained in shallow caries, suggesting a type 1 cytokine mechanism in early pulpitis where S. mutans predominates. In contrast, in deep caries no differences in cytokine frequency were observed. Furthermore, the presence of IFN-gamma in the pulp correlated with the presence of S. mutans. The extraordinary induction of type 1 cytokines and the preferential activation of CD8+ T cells by S. mutans offers an explanation for the etiology of the CD8+ T-cell-dominant lesion in early pulpitis and suggests that S. mutans may have a major impact on the initial lesion and pulpal pathology.

* Corresponding author. Mailing address: Department of Endodontics, P.O. Box 980556, MCV/VCU, Richmond, VA 23298-0556. Phone: (804) 828-0784. Fax: (804) 828-4913. E-mail: chahn{at}hsc.vcu.edu.

Infection and Immunity, December 2000, p. 6785-6789, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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