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Treponema denticola: FhbB, Dentilisin, Complement Evasion and the Paradox of Factor H Cleavage

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The Pathogenic Spirochetes: strategies for evasion of host immunity and persistence

Abstract

Treponema denticola transitions from being relatively low in number in the sub-gingival crevice of healthy individuals to being abundant in periodontal pockets. The abundance of T. denticola correlates with periodontal disease severity. To thrive in periodontal pockets, the ability to evade complement mediated destruction is essential. Consistent with this, T. denticola can survive exposure to serum concentrations as high as 25 %. The binding of Factor H (FH; a negative regulator of the complement system) by the T. denticola surface protein, FhbB, serves as the primary mechanism of serum resistance. While numerous other pathogens exploit the negative regulatory activity of FH in immune evasion, the FH–T. denticola interaction is unique. Bound FH is cleaved by the T. denticola protease, dentilisin (a chymotrypsin like-protease complex). In this chapter, we summarize our current understanding of the complement evasion strategies of T. denticola and discuss the hypothesis that FH cleavage by T. denticola locally dysregulates the complement system resulting in conditions that favor microbial growth and the progression of periodontal disease.

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Correspondence to Richard T. Marconi Ph.D. .

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McDowell, J.V., Miller, D.P., Mallory, K.L., Marconi, R.T. (2012). Treponema denticola: FhbB, Dentilisin, Complement Evasion and the Paradox of Factor H Cleavage. In: Embers, M. (eds) The Pathogenic Spirochetes: strategies for evasion of host immunity and persistence. Springer, Boston, MA. https://doi.org/10.1007/978-1-4614-5404-5_3

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