Affiliation: University of Washington
- Porphyromonas gingivalis as a potential community activist for diseaseR P Darveau
University of Washington, 1959 NE Pacific Street, Room D 570, UW Mailbox 357444, Seattle, WA 98195 7444, USA
J Dent Res 91:816-20. 2012..Thus, P. gingivalis creates a dysbiosis between the host and dental plaque, and this may represent one mechanism by which periodontitis can be initiated. We have therefore termed P. gingivalis a keystone pathogen...
- Periodontitis: a polymicrobial disruption of host homeostasisRichard P Darveau
University of Washington, Seattle, Washington 98195, USA
Nat Rev Microbiol 8:481-90. 2010..Furthermore, disease may result from 'community-based' attack on the host. Here, I describe the interaction of the host immune system with the oral bacteria in healthy states and in diseased states...
- The oral microbial consortium's interaction with the periodontal innate defense systemRichard P Darveau
Department of Periodontics, University of Washington, Seattle, 98195 7444, USA
DNA Cell Biol 28:389-95. 2009....
- Local chemokine paralysis, a novel pathogenic mechanism for Porphyromonas gingivalisR P Darveau
Bristol Myers Squibb Pharmaceutical Research Institute, Seattle, Washington 98121, USA
Infect Immun 66:1660-5. 1998..gingivalis colonization (local chemokine paralysis) will severely impair mucosal defense and represents a novel mechanism for bacterial colonization of host tissue...
- Porphyromonas gingivalis lipopolysaccharide contains multiple lipid A species that functionally interact with both toll-like receptors 2 and 4Richard P Darveau
Department of Periodontics, University of Washington, Health Sciences Center, Box 357444, Seattle, WA 98195, USA
Infect Immun 72:5041-51. 2004..gingivalis LPS preparations is not currently understood, it is proposed that the presence of multiple lipid A species contributes to cell activation through both TLR2 and TLR4...
- Porphyromonas gingivalis lipopolysaccharide is both agonist and antagonist for p38 mitogen-activated protein kinase activationRichard P Darveau
Department of Periodontics, University of Washington, Seattle, Washington 98181, USA
Infect Immun 70:1867-73. 2002..These data also suggest that although LPS is generally considered a bacterial component that alerts the host to infection, LPS from P. gingivalis may selectively modify the host response as a means to facilitate colonization...
- Lipid A diversity and the innate host response to bacterial infectionR P Darveau
Department of Periodontics, Box 357444, School of Dentistry, Universityof Washington, Seattle, WA 98195 7444, USA
Curr Opin Microbiol 1:36-42. 1998..Recent data indicate that bacteria can regulate this molecule in response to different host microenvironments. Host factors that induce lipid A modifications and the resultant changes in host response remain to be determined...
- Porphyromonas gingivalis lipopolysaccharide lipid A heterogeneity: differential activities of tetra- and penta-acylated lipid A structures on E-selectin expression and TLR4 recognitionRobert A Reife
Department of Periodontics, University of Washington, Seattle, WA 98195, USA
Cell Microbiol 8:857-68. 2006..gingivalis LPS, with opposing effects on the E-selectin response suggests that this organism is able to modulate innate host responses by alterations in the relative amount of these lipid A structures...
- Porphyromonas gingivalis lipopolysaccharide displays functionally diverse interactions with the innate host defense systemBrian W Bainbridge
Department of Periodontics, University of Washington, Seattle, Washington 98195, USA
Ann Periodontol 7:29-37. 2002..We speculate that P. gingivalis lipid A structural heterogeneity contributes to the unusual innate host response to this LPS and its ability to interact with different TLR molecules...
- Expression of a Porphyromonas gingivalis lipid A palmitylacyltransferase in Escherichia coli yields a chimeric lipid A with altered ability to stimulate interleukin-8 secretionBrian W Bainbridge
Department of Oral Biology, University of Washington, Seattle, WA 98195, USA
Cell Microbiol 8:120-9. 2006..coli lipid A altered the activity of the LPS in monocytes but not endothelial cell assays and the difference in recognition does not appear to be related to differences in Toll-like receptor utilization...
- Correlates of periodontal decline and biologic markers in older adultsJessica R Swoboda
Department of Periodontics, University of Washington, Seattle, WA, USA
J Periodontol 79:1920-6. 2008..This study measured bacterial and serum cytokine and high-sensitivity C-reactive protein (hsCRP) levels in older persons...
- Porphyromonas gingivalis resistance to polymyxin B is determined by the lipid A 4'-phosphatase, PGN_0524Stephen R Coats
Department of Periodontics, School of Dentistry, University of Washington, Seattle, Washington 98195, USA
Int J Oral Sci 1:126-35. 2009..To elucidate the genetic basis for the pronounced resistance that the oral pathogen, Porphyromonas gingivalis (P. gingivalis), exhibits towards the cationic antimicrobial peptide, polymyxin B...
- MD-2 mediates the ability of tetra-acylated and penta-acylated lipopolysaccharides to antagonize Escherichia coli lipopolysaccharide at the TLR4 signaling complexStephen R Coats
Department of Periodontics, University of Washington School of Dentistry, Seattle 98195, USA
J Immunol 175:4490-8. 2005..However, MD-2 represents the principal molecular component that tetra-acylated P. gingivalis LPS and penta-acylated msbB LPS use to antagonize hexa-acylated E. coli LPS at the TLR4 signaling complex...
- The lipid A phosphate position determines differential host Toll-like receptor 4 responses to phylogenetically related symbiotic and pathogenic bacteriaStephen R Coats
Department of Periodontics, School of Dentistry, University of Washington, 1959 NE Pacific St, HSB, Box 357444, Seattle, WA 98195, USA
Infect Immun 79:203-10. 2011..We propose that the distinct lipid A phosphate positions observed for the B. thetaiotaomicron and P. gingivalis LPS contributes to the manifestation of these bacteria as commensal or pathogen within the human host...
- Porphyromonas gingivalis lipopolysaccharide antagonizes Escherichia coli lipopolysaccharide at toll-like receptor 4 in human endothelial cellsStephen R Coats
Department of Periodontics, University of Washington, Seattle, Washington 98195, USA
Infect Immun 71:6799-807. 2003..gingivalis LPS-dependent antagonism of E. coli LPS in human endothelial cells likely involves the ability of P. gingivalis LPS to directly compete with E. coli LPS at the TLR4 signaling complex...
- Oral and serum IL-6 levels in oral lichen planus patientsGao Man Gu
Dept of Orthodontics, School of Dentistry, University of Washington, Seattle, USA
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 98:673-8. 2004..Venous blood was processed to serum for ELISA assay. Oral IL-6 was expressed as both pg/mL and pg/mug protein, and serum IL-6 was expressed as pg/mL...
- Human Toll-like receptor 4 responses to P. gingivalis are regulated by lipid A 1- and 4'-phosphatase activitiesStephen R Coats
Department of Periodontics, School of Dentistry, University of Washington, 1959 NE Pacific St, Seattle, WA 98195 7444, USA
Cell Microbiol 11:1587-99. 2009..gingivalis lipid A activity from TLR4 evasive to TLR4 suppressive, potentially altering critical interactions between this bacterium, the local microbial community and the host innate immune system...
- Modulation of the innate immune response within the periodontiumDouglas R Dixon
United States Army Dental Corps and Department of Periodontics and Oral Biology, School of Dentistry, University of Washington, Seattle, USA
Periodontol 2000 35:53-74. 2004
- Antagonistic lipopolysaccharides block E. coli lipopolysaccharide function at human TLR4 via interaction with the human MD-2 lipopolysaccharide binding siteStephen R Coats
Department of Periodontics, University of Washington School of Dentistry, Seattle, WA 98195, USA
Cell Microbiol 9:1191-202. 2007..coli lipopolysaccharide-hMD-2 complexes function at hTLR4. It is also shown that both hTLR4 and hMD-2 contribute to the species-specific recognition of msbB and P. gingivalis lipopolysaccharides as antagonists at the hTLR4 complex...
- The structurally similar, penta-acylated lipopolysaccharides of Porphyromonas gingivalis and Bacteroides elicit strikingly different innate immune responsesAlex B Berezow
Department of Microbiology, University of Washington School of Medicine, Seattle, WA 98195, USA
Microb Pathog 47:68-77. 2009..Further, we show the difference in potency between Bacteroides and P. gingivalis LPS is TLR4-dependent. Altogether, the data suggest subtle changes in lipid A structure may profoundly impact the host's innate immune response...
- Hemin-dependent modulation of the lipid A structure of Porphyromonas gingivalis lipopolysaccharideMontaser N Al-Qutub
Department of Periodontics, University of Washington, Box 357444, Seattle, Washington 98195, USA
Infect Immun 74:4474-85. 2006..gingivalis lipid A structures have opposing effects on Toll-like receptor 4 activation, the alteration of the lipid A structural content may have significant effects on the host response to this bacterium...
- Hierarchical gene expression profiles of HUVEC stimulated by different lipid A structures obtained from Porphyromonas gingivalis and Escherichia coliCasey Chen
Department of Periodontics and Oral Biology, University of Washington, Seattle, WA 98195, USA
Cell Microbiol 9:1028-38. 2007..A unique gene expression profile for the weak TLR4 agonist PgLPS(1690) was observed and represents a TLR4 hierarchy in endothelial cell gene activation...
- Acyl chain specificity of the acyltransferases LpxA and LpxD and substrate availability contribute to lipid A fatty acid heterogeneity in Porphyromonas gingivalisBrian W Bainbridge
Department of Periodontics and Oral Biology and Medicine, University of Washington, D 652 Health Sciences Building, 1959 NE Pacific St, Seattle, Washington 98195 7444, USA
J Bacteriol 190:4549-58. 2008..gingivalis lipid A acyltransferases and the substrate availability account for the lipid A structural clusters that differ by 14 mass units observed in P. gingivalis lipopolysaccharide preparations...
- Antimicrobial photodynamic therapy may promote periodontal healing through multiple mechanismsPam Braham
Department of Periodontics, University of Washington, Seattle, WA 98195 7444, USA
J Periodontol 80:1790-8. 2009..It also inactivates host destructive cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-1 beta...
- P. gingivalis and E. coli lipopolysaccharides exhibit different systemic but similar local induction of inflammatory markersRongkun Liu
Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
J Periodontol 79:1241-7. 2008..gingivalis lipopolysaccharide (PgLPS), PgLPS(1435)(/1449) and PgLPS(1690), exhibit differences in their capacity to stimulate systemic versus local responses compared to Escherichia coli lipopolysaccharide (LPS)...
- The expression profile of lipopolysaccharide-binding protein, membrane-bound CD14, and toll-like receptors 2 and 4 in chronic periodontitisLei Ren
Faculty of Dentistry, Periodontology, The University of Hong Kong, Hong Kong Special Administrative Region, China
J Periodontol 76:1950-9. 2005..Altered cellular expression profiles of mCD14 and TLR 2 and 4 in periodontal pocket tissues imply that these pattern recognition receptors may play a role in periodontal pathogenesis...
- Mouse paneth cell secretory responses to cell surface glycolipids of virulent and attenuated pathogenic bacteriaHiroki Tanabe
Department of Pathology, School of Medicine, College of Health Sciences, University of California, Irvine, CA 92697-4800, USA
Infect Immun 73:2312-20. 2005..Thus, mouse Paneth cells respond equivalently to purified bacterial cell envelope glycolipids, regardless of functional Tlr4, the structural properties of glycolipid acyl chains, or their association with virulence in humans...
- The in vivo expression of membrane-bound CD14 in periodontal health and diseaseLijian Jin
Faculty of Dentistry, Periodontology, The University of Hong Kong, Hong Kong
J Periodontol 75:578-85. 2004..This study investigated the in vivo expression profile and levels of mCD14 in healthy and diseased gingival tissues...
- Oral Commensal Bacterial Modulation of the Periodontal Innate Host ResponseRichard Darveau; Fiscal Year: 2007....
- P Gingivalis LPS: Hemin-induced lipid A structural remodellingRICHARD PETERS DARVEAU; Fiscal Year: 2010..We suspect the modulation of the host immune response contributes to its ability to cause disease. ..
- P. GINGIVALIS LPS-MODULATION OF INNATE HOST DEFENSERichard Darveau; Fiscal Year: 2007..gingivalis lipid A diversity is generated. The third Aim will examine potential TLR mediated innate host interactions of the different lipid A species generated in Aims 1 and 2. ..
- P. gingivalis lipid A species modulation of endothelial cell gene activation progRichard Darveau; Fiscal Year: 2007..gingivalis interactions with TLR4 or other novel LPS receptors. Furthermore, the microarray analysis results will be made public by deposition at the European Bioinformatics Institute Array Express database. ..
- Oral Commensal Bacterial Modulation of the Periodontal Innate Host ResponseRICHARD PETERS DARVEAU; Fiscal Year: 2010....
- ASM Conf. on Beneficial Microbial Symbionts in AnimalsRichard Darveau; Fiscal Year: 2005..It is an intellectually stimulating subject that attracts pioneering graduate students and post-doctoral fellows who will benefit from participation in a focused and dynamic conference; ..
- LBP/CD14 interactions with bacterial componentsRichard Darveau; Fiscal Year: 2005..These studies will provide further insight into how the innate host defense system recognizes and responds to different bacteria, a key component of both oral health and disease. ..
- PGINGIVALIS LPS--INHIBITION OF INNATE HOST DEFENSERichard Darveau; Fiscal Year: 2002..The overall goal of this application is to identify new therapies based upon this unique virulence characteristic of P. gingivalis LPS. ..