Complement and Dysbiosis in Periodontal Disease

Immunobiology. 2012 Nov;217(11):1111-6. doi: 10.1016/j.imbio.2012.07.007.

Abstract

Signaling crosstalk between complement and Toll-like receptors (TLRs) normally serves to coordinate host immunity. However, the periodontal bacterium Porphyromonas gingivalis expresses C5 convertase-like enzymatic activity and adeptly exploits complement-TLR crosstalk to subvert host defenses and escape elimination. Intriguingly, this defective immune surveillance leads to the remodeling of the periodontal microbiota to a dysbiotic state that causes inflammatory periodontitis. Understanding the mechanisms by which P. gingivalis modulates complement function to cause dysbiosis offers new targets for complement therapeutics.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Bacteroidaceae Infections / immunology
  • Bacteroidaceae Infections / metabolism
  • Bacteroidaceae Infections / microbiology
  • Complement Activation*
  • Complement C3-C5 Convertases / metabolism*
  • Complement System Proteins / immunology*
  • Humans
  • Microbial Interactions
  • Periodontitis / immunology*
  • Periodontitis / metabolism
  • Periodontitis / microbiology*
  • Porphyromonas gingivalis / enzymology
  • Porphyromonas gingivalis / metabolism
  • Porphyromonas gingivalis / pathogenicity*
  • Signal Transduction
  • Toll-Like Receptors / metabolism*

Substances

  • Toll-Like Receptors
  • Complement System Proteins
  • Complement C3-C5 Convertases