Journal
INFECTION AND IMMUNITY
Volume 70, Issue 7, Pages 3982-3984Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.70.7.3982-3984.2002
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Funding
- NIDCR NIH HHS [T32 DE 07063, T32 DE007063] Funding Source: Medline
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Spirochetes, including Treponema denticola, are implicated in the pathogenesis of periodontal disease. Because T. denticola lacks lipopolysaccharides that serve as targets for human beta-defensin (hbetaD) binding, we postulated that T. denticola would resist killing by hbetaD. We showed that T. denticola is resistant to hbetaD-1 and -2. Protease inhibitors did not enhance killing of T. denticola by hbetaD-2, suggesting that degradation of hbetaD-2 by treponemal proteases is not a major factor in T. denticola resistance.
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