Low-abundance biofilm species orchestrates inflammatory periodontal disease through the commensal microbiota and complement.

[1]  P. Allen,et al.  Commensal Bacteroides species induce colitis in host-genotype-specific fashion in a mouse model of inflammatory bowel disease. , 2011, Cell host & microbe.

[2]  Elizabeth A. Grice,et al.  The skin microbiome , 2020, Nature.

[3]  A. Darzi,et al.  Gut microbiome-host interactions in health and disease , 2011, Genome Medicine.

[4]  John D. Lambris,et al.  Microbial manipulation of receptor crosstalk in innate immunity , 2011, Nature Reviews Immunology.

[5]  John D Lambris,et al.  The C5a Receptor Impairs IL-12–Dependent Clearance of Porphyromonas gingivalis and Is Required for Induction of Periodontal Bone Loss , 2011, The Journal of Immunology.

[6]  G. Trinchieri,et al.  Innate immune mechanisms of colitis and colitis-associated colorectal cancer , 2011, Nature Reviews Immunology.

[7]  G. Hajishengallis Complement and periodontitis. , 2010, Biochemical pharmacology.

[8]  K. Lundberg,et al.  Periodontitis in RA—the citrullinated enolase connection , 2010, Nature Reviews Rheumatology.

[9]  F. Syed,et al.  Integrative physiology of the aging bone: insights from animal and cellular models , 2010, Annals of the New York Academy of Sciences.

[10]  Maria Karlsson,et al.  Enterobacteriaceae act in concert with the gut microbiota to induce spontaneous and maternally transmitted colitis. , 2010, Cell host & microbe.

[11]  John D Lambris,et al.  Complement: a key system for immune surveillance and homeostasis , 2010, Nature Immunology.

[12]  R. Genco,et al.  Prevention: Reducing the risk of CVD in patients with periodontitis , 2010, Nature Reviews Cardiology.

[13]  R. Lamont,et al.  Role of Porphyromonas gingivalis Phosphoserine Phosphatase Enzyme SerB in Inflammation, Immune Response, and Induction of Alveolar Bone Resorption in Rats , 2010, Infection and Immunity.

[14]  R. Darveau,et al.  Periodontitis: a polymicrobial disruption of host homeostasis , 2010, Nature Reviews Microbiology.

[15]  J. Lambris,et al.  Crosstalk pathways between Toll-like receptors and the complement system. , 2010, Trends in immunology.

[16]  A. Macpherson,et al.  Immune adaptations that maintain homeostasis with the intestinal microbiota , 2010, Nature Reviews Immunology.

[17]  John D Lambris,et al.  Microbial Hijacking of Complement–Toll-Like Receptor Crosstalk , 2010, Science Signaling.

[18]  P. Zipfel,et al.  Complement regulators and inhibitory proteins , 2009, Nature Reviews Immunology.

[19]  Thomas F. Tedder,et al.  Innate and Adaptive Immunity Cooperate Flexibly to Maintain Host-Microbiota Mutualism , 2009, Science.

[20]  G. Hajishengallis Porphyromonas gingivalis-host interactions: open war or intelligent guerilla tactics? , 2009, Microbes and infection.

[21]  John D. Lambris,et al.  Modulation of the anti-tumor immune response by complement , 2008, Nature Immunology.

[22]  M. Hattori,et al.  Determination of the Genome Sequence of Porphyromonas gingivalis Strain ATCC 33277 and Genomic Comparison with Strain W83 Revealed Extensive Genome Rearrangements in P. gingivalis , 2008, DNA research : an international journal for rapid publication of reports on genes and genomes.

[23]  D. Graves,et al.  The use of rodent models to investigate host-bacteria interactions related to periodontal diseases. , 2008, Journal of clinical periodontology.

[24]  Michael D. Connolly,et al.  Use of Ly6G‐specific monoclonal antibody to deplete neutrophils in mice , 2008, Journal of leukocyte biology.

[25]  G. Dougan,et al.  Salmonella enterica Serovar Typhimurium Exploits Inflammation to Compete with the Intestinal Microbiota , 2007, PLoS biology.

[26]  B. Finlay,et al.  Host-mediated inflammation disrupts the intestinal microbiota and promotes the overgrowth of Enterobacteriaceae. , 2007, Cell host & microbe.

[27]  F. Yoshimura,et al.  Fimbrial Proteins of Porphyromonas gingivalis Mediate In Vivo Virulence and Exploit TLR2 and Complement Receptor 3 to Persist in Macrophages1 , 2007, The Journal of Immunology.

[28]  R. Page,et al.  Immunization of Macaca fascicularis against experimental periodontitis using a vaccine containing cysteine proteases purified from Porphyromonas gingivalis. , 2007, Oral microbiology and immunology.

[29]  Francesco D'Aiuto,et al.  Treatment of periodontitis and endothelial function. , 2007, The New England journal of medicine.

[30]  N. Slakeski,et al.  Kgp and RgpB, but Not RgpA, Are Important for Porphyromonas gingivalis Virulence in the Murine Periodontitis Model , 2007, Infection and Immunity.

[31]  M. Moeschberger,et al.  Changes in Periodontal Health Status Are Associated with Bacterial Community Shifts as Assessed by Quantitative 16S Cloning and Sequencing , 2006, Journal of Clinical Microbiology.

[32]  A. Gallagher,et al.  Structural analysis of a novel anionic polysaccharide from Porphyromonas gingivalis strain W50 related to Arg‐gingipain glycans , 2005, Molecular microbiology.

[33]  B. Ebenman,et al.  Using community viability analysis to identify fragile systems and keystone species. , 2005, Trends in ecology & evolution.

[34]  Ryan T Demmer,et al.  Periodontal Microbiota and Carotid Intima-Media Thickness: The Oral Infections and Vascular Disease Epidemiology Study (INVEST) , 2005, Circulation.

[35]  J. H. Brown,et al.  Complex species interactions and the dynamics of ecological systems: long-term experiments. , 2001, Science.

[36]  M. Jeffcoat,et al.  Persistent bacterial colonization of Porphyromonas gingivalis, Prevotella intermedia, and Actinobacillus actinomycetemcomitans in periodontitis and its association with alveolar bone loss after 6 months of therapy. , 2000, Journal of clinical periodontology.

[37]  D. Roopenian,et al.  Genetic Control of Susceptibility toPorphyromonas gingivalis-Induced Alveolar Bone Loss in Mice , 2000, Infection and Immunity.

[38]  C. Douglas,et al.  Enumeration of Porphyromonas gingivalis, Prevotella intermedia and Actinobacillus actinomycetemcomitans in subgingival plaque samples by a quantitative-competitive PCR method. , 2000, Journal of medical microbiology.

[39]  Z. Ding,et al.  Relative contribution of LFA-1 and Mac-1 to neutrophil adhesion and migration. , 1999, Journal of immunology.

[40]  D. Craik,et al.  Low-molecular-weight peptidic and cyclic antagonists of the receptor for the complement factor C5a. , 1999, Journal of medicinal chemistry.

[41]  N. Lang,et al.  Neutrophil migration into the gingival sulcus is associated with transepithelial gradients of interleukin-8 and ICAM-1. , 1998, Journal of periodontology.

[42]  C. M. Belton,et al.  Local Chemokine Paralysis, a Novel Pathogenic Mechanism for Porphyromonas gingivalis , 1998, Infection and Immunity.

[43]  J. Castilla,et al.  Challenges in the Quest for Keystones , 1996 .

[44]  J. G. Fisher,et al.  Inactivation of the Porphyromonas gingivalis fimA gene blocks periodontal damage in gnotobiotic rats , 1994, Journal of bacteriology.

[45]  R. Genco,et al.  Immunization with Porphyromonas (Bacteroides) gingivalis fimbriae protects against periodontal destruction , 1992, Infection and immunity.

[46]  N. Lang,et al.  Assessment of complement cleavage in gingival fluid during experimental gingivitis in man. , 1989, Journal of clinical periodontology.

[47]  S. Holt,et al.  Implantation of Bacteroides gingivalis in nonhuman primates initiates progression of periodontitis. , 1988, Science.

[48]  A. C. Johannessen,et al.  Deposits of immunoglobulins, complement, and immune complexes in inflamed human gingiva. , 1987, Acta odontologica Scandinavica.

[49]  R. Genco,et al.  Gingival fluid and serum in periodontal diseases. II. Evidence for cleavage of complement components C3, C3 proactivator (factor B) and C4 in gingival fluid. , 1977, Journal of periodontology.

[50]  W. Ketterl [Periodontal diseases]. , 1971, Der Zahnarzt; Colloquium med. dent.