Treponema denticola is resistant to human beta-defensins.
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 (h beta D) binding, we postulated that T. denticola would resist killing by h beta D. We showed that T. denticola is resistant to h beta D-1 and -2. Protease inhibitors did not enhance killing of T. denticola by h beta D-2, suggesting that degradation of h beta D-2 by treponemal proteases is not a major factor in T. denticola resistance.
Brissette
Catherine A
CA
Department of Pathobiology, University of Washington, Seattle, Washington 98195, USA.
Lukehart
Sheila A
SA
D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D004396:Coloring Agents / Q000378:metabolism; D024881:Drug Resistance, Bacterial; D006801:Humans; D009842:Oligopeptides / Q000494:pharmacology; D010078:Oxazines; D015842:Serine Proteinase Inhibitors / Q000494:pharmacology; D014208:Treponema / Q000187:drug effects* / Q000378:metabolism; D014966:Xanthenes; D023083:beta-Defensins / Q000494:pharmacology*
D000900:Anti-Bacterial Agents; D004396:Coloring Agents; C406407:DEFB1 protein, human; C106641:DEFB4A protein, human; D009842:Oligopeptides; D010078:Oxazines; D015842:Serine Proteinase Inhibitors; D014966:Xanthenes; D023083:beta-Defensins; C005843:resazurin; C002101:chymostatin