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Infection and Immunity, July 2004, p. 4102-4108, Vol. 72, No. 7
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.7.4102-4108.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

S100 and Cytokine Expression in Caries

Julia L. McLachlan,1 Alastair J. Sloan,1 Anthony J. Smith,1 Gabriel Landini,2 and Paul R. Cooper1*

Oral Biology,1 Oral Pathology, School of Dentistry, The University of Birmingham, Birmingham B4 6NN, United Kingdom2

Received 19 November 2003/ Returned for modification 26 January 2004/ Accepted 11 March 2004

The molecular immune response of the pulpal tissue during chronic carious infection is poorly characterized. Our objective was to examine the expression of potential molecular mediators of pulpal inflammation, correlate their levels with disease severity, and determine the cellular localization of key molecules. Results indicated that there was significantly increased transcriptional activity in carious compared to healthy pulp, and the increase correlated positively with disease severity. Semiquantitative reverse transcriptase PCR analysis in 10 carious and 10 healthy pulpal tissue samples of the S100 family members S100A8, S100A9, S100A10, S100A12, and S100A13; the cytokines tumor necrosis factor alpha (TNF-{alpha}), interleukin-1ß (IL-1ß), IL-8, IL-6, and epithelial cell-derived neutrophil attractant 78 (ENA-78); and the structural protein collagen-1{alpha} indicated that all genes tested, with the exception of S100A10, were more abundantly expressed in carious teeth. In addition, we found that the closer the carious lesion front was to the pulpal chamber the higher the expression was for all genes except S100A10. Multiple-regression analysis identified a significant positive correlation between the expression levels of S100A8 and IL-1ß, ENA-78, and IL-6 and between collagen-1{alpha} and S100A8, TNF-{alpha}, IL-1ß, IL-8, IL-6, and ENA-78. Immunohistochemical studies in carious pulpal tissue indicated that S100A8 and the S100A8/S100A9 complex were predominantly expressed by infiltrating neutrophils. Gene expression analyses in immune system cells supported these findings and indicated that bacterial activation of neutrophils caused upregulation of S100A8, S100A9, and S100A13. This study highlights the complex nature of the molecular immune response that occurs during carious infection.

* Corresponding author. Mailing address: Oral Biology, School of Dentistry, The University of Birmingham, Birmingham B4 6NN, United Kingdom. Phone: 121 237 2785. Fax: 121 237 2882. E-mail: p.r.cooper.1{at}bham.ac.uk.

Editor: A. D. O'Brien

Infection and Immunity, July 2004, p. 4102-4108, Vol. 72, No. 7
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.7.4102-4108.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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