title: Complement and dysbiosis in periodontal disease.
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.
authors.affiliation: University of Pennsylvania School of Dental Medicine, Department of Microbiology, Philadelphia, PA 19104, USA. geoh@upenn.edu
authors.forename: George
authors.initials: G
authors.lastname: Hajishengallis
authors.forename: John D
authors.initials: JD
authors.lastname: Lambris
mesh_terms: D016866:Bacteroidaceae Infections / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D003167:Complement Activation; D050577:Complement C3-C5 Convertases / Q000378:metabolism*; D003165:Complement System Proteins / Q000276:immunology*; D006801:Humans; D056265:Microbial Interactions; D010518:Periodontitis / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology*; D016966:Porphyromonas gingivalis / Q000201:enzymology / Q000378:metabolism / Q000472:pathogenicity*; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000378:metabolism*
chemical_list: D051193:Toll-Like Receptors; D003165:Complement System Proteins; D050577:Complement C3-C5 Convertases