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J. Biol. Chem., Vol. 277, Issue 19, 16599-16605, May 10, 2002
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From the Fluoridation causes an obvious reduction of
dental caries by interference with cariogenic streptococci. However,
the effect of fluoride on group A streptococci that causes rheumatic
fever and acute poststreptococcal glomerulonephritis is not known. We have used proteomic analysis to create a reference proteome map for
Streptococcus pyogenes and to determine fluoride-induced
protein changes in the streptococci. Cellular and extracellular
proteins were resolved by two-dimensional polyacrylamide gel
electrophoresis and identified by matrix-assisted laser desorption
ionization mass spectrometry. 183 protein spots were visualized, and 74 spots representing 60 unique proteins were identified. A 16-h exposure to sodium fluoride caused decreased expression of proteins required to
respond to cellular stress, including anti-oxidants, glycolytic enzymes, transcriptional and translational regulators, and protein folding. Fluoride caused decreased cellular expression of two well-characterized S. pyogenes virulence factors. Fluoride
decreased expression of glyceraldehyde-3-phosphate dehydrogenase, which acts to bind fibronectin and promote bacterial adherence. We also performed proteomic analysis of protein released by S. pyogenes into the culture supernatant and observed decreased
expression of M proteins following fluoride exposure. These data
provide evidence that fluoride causes decreased expression by S. pyogenes proteins used to respond to stress, virulence factors,
and implicated in non-suppurative complications of S. pyogenes, including glomerulonephritis and rheumatic fever.
Fluoride Exposure Attenuates Expression of Streptococcus
pyogenes Virulence Factors*
§¶,
,,§§¶¶, and
Core Proteomics Laboratory, Kidney Disease
Program, Department of Medicine, University of Louisville, Louisville,
Kentucky 40202, the § Department of Medicine, Faculty of
Medicine, Chiang Mai University, Chiang Mai 50200, Thailand, the
Department of Microbiology and Immunology, University of
Louisville, Louisville, Kentucky 40202, the
Veterans Administration Medical Center,
Louisville, Kentucky, the ¶¶ Department of Biochemistry
and Molecular Biology, University of Louisville, Louisville, Kentucky
40202, and the ** Department of Pharmacology and
Toxicology, University of Louisville, Louisville, Kentucky 40202
*
This work was supported in part by grants from the
Department of Veterans Affairs (to J. B. K.), National Institutes of
Health Grant R01 HL66358-01, and the Jewish Hospital Foundation,
Louisville, KY.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Posthumous.
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