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Infection and Immunity, March 2002, p. 1113-1120, Vol. 70, No. 3
0019-9567/02/$04.00+0 DOI: 10.1128/IAI.70.3.1113-1120.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Departments of Periodontics,1 Pathology, University of Texas Health Science Center, San Antonio, Texas 78229 ,2 Center for Oral Health Research, University of Kentucky, Lexington, Kentucky 405363
Received 16 August 2001/ Returned for modification 24 October 2001/ Accepted 19 November 2001
Hydrogen sulfide (H2S) is a major metabolic end product detected in deep periodontal pockets that is produced by resident periodontopathic microbiota associated with the progression of periodontitis. Treponema denticola, a member of the subgingival biofilm at disease sites, produces cystalysin, an enzyme that catabolizes cysteine, releasing H2S. The metabolic pathway leading to H2S formation in periodontal pockets has not been determined. We used a variety of thiol compounds as substrates for T. denticola to produce H2S. Our results indicate that glutathione, a readily available thiol source in periodontal pockets, is a suitable substrate for H2S production by this microorganism. In addition to H2S, glutamate, glycine, ammonia, and pyruvate were metabolic end products of metabolism of glutathione. Cysteinyl glycine (Cys-Gly) was also catabolized by the bacteria, yielding glycine, H2S, ammonia, and pyruvate. However, purified cystalysin could not catalyze glutathione and Cys-Gly degradation in vitro. Moreover, the enzymatic activity(ies) in T. denticola responsible for glutathione breakdown was inactivated by trypsin or proteinase K, by heating (56°C) and freezing (-20°C), by sonication, and by exposure to N
-p-tosyl-L-lysine chloromethyl ketone (TLCK). These treatments had no effect on degradation of cysteine by the purified enzyme. In this study we delineated an enzymatic pathway for glutathione metabolism in the oral spirochete T. denticola; our results suggest that glutathione metabolism plays a role in bacterial nutrition and potential virulence expression.
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