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Periodontal Pathogen Porphyromonas Gingivalis (periodontal + pathogen_porphyromona_gingivali)
Selected AbstractsThe effect of immunization on the response to P. gingivalis infection in mice is adjuvant-dependentJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 9 2005Yael Houri-Haddad Abstract Aim: Studies on vaccines against the periodontal pathogen Porphyromonas gingivalis have produced conflicting results, but no consideration has been given to the role of different adjuvants in these vaccines. We have previously shown that an intra-chamber challenge with heat-killed P. gingivalis was modified by immunization with different adjuvants. This study tested the hypothesis that different adjuvants in P. gingivalis vaccines would differentially modify the host response to a live P. gingivalis infection. Results: Using P. gingivalis -infected subcutaneous chambers in mice, we show that vaccination with P. gingivalis in alum attenuated the pro-inflammatory cytokine levels at the site of infection, while the vaccine containing incomplete Freund's adjuvant did the opposite. Although both vaccines induced a similar humoral IgG response, P. gingivalis -induced abscesses were significantly smaller in the alum-adjuvant group. Conclusions: The results suggest that the immune response and the resultant protection to a P. gingivalis infection, in P. gingivalis -vaccinated mice, are adjuvant-dependent. [source] Binding of the periodontitis associated bacterium Porphyromonas gingivalis to glycoproteins from human epithelial cellsMOLECULAR ORAL MICROBIOLOGY, Issue 5 2008U. Hallén Introduction:, In the present study we examined the ability of the periodontal pathogen Porphyromonas gingivalis to adhere to glycoconjugates on intact cells and to protein preparations of epithelial cells (KB cells). Methods:, The KB cell protein preparation was separated by sodium dodecyl sulfate,polyacrylamide gel electrophoresis and transferred to nitrocellulose membranes by Western blotting. The membranes were used in overlay assays with labeled P. gingivalis. Flow cytometry was used to analyze attachment of bacteria to intact KB cells. Results:, Glycoconjugate expression on the KB cells and in the protein preparation was confirmed. Binding was detected to several bands on the Western blots. Flow cytometry showed a distinct increase in fluorescence for strain FDC 381. Preincubation of the bacteria with mannose, fucose, N -acetylglucosamine and N -acetylgalactosamine inhibited the binding to KB cells by approximately 30% whereas preincubation with N -acetylneuraminic acid reduced the binding by 60%. Conclusion:, These results indicate that carbohydrate structures are involved in the binding process of P. gingivalis to oral epithelial cells and that neuraminic acid plays a significant role in the adhesion process. [source] Signaling pathways in osteoblast proinflammatory responses to infection by Porphyromonas gingivalisMOLECULAR ORAL MICROBIOLOGY, Issue 2 2008T. Ohno Introduction:, We recently investigated global gene expression in ST2 mouse stromal cells infected by the periodontal pathogen Porphyromonas gingivalis using microarray technology, and found that the bacterium induces a wide range of proinflammatory gene expression. Here, we reported the signaling pathways involved in those proinflammatory responses. Methods:, ST2 cells and primary calvarial osteoblasts from C3H/HeN, C57BL/6, and MyD88-deficient (MyD88,/,) mice were infected with P. gingivalis ATCC33277 and its gingipain-deficient mutant KDP136. Expression of the chemokines CCL5 and CXCL10, and matrix metalloproteinase-9 (MMP9) were quantified by real-time polymerase chain reaction, while phosphorylation of protein kinases and degradation of an inhibitor of nuclear factor-,B, I,B-,, were detected by Western blotting, and activation of transcriptional factors was determined by a luciferase reporter assay. The effects of inhibitors of transcriptional factors and protein kinases were also investigated. Results:, Infection by P. gingivalis elicited gene expression of CCL5, CXCL10, and MMP9 in both ST2 cells and osteoblasts. Western blot and reporter assay results revealed activation of nuclear factor-,B (NF-,B) and activator protein-1 transcription factors. The NF-,B inhibitor suppressed the expression of CCL5 and MMP9, but not that of CXCL10, whereas P. gingivalis infection induced significant CCL5 expression in MyD88,/, osteoblasts. In addition, activation of protease-activated receptors by trypsin elicited significant induction of CXCL10. Conclusion:, Our results suggest that various proinflammatory responses in P. gingivalis -infected stromal/osteoblast cells are NF-,B-dependent, but not always dependent on the Toll-like receptor/MyD88 pathway, while some responses are related to the activation of protease-activated receptors. Thus, P. gingivalis does not fully utilize well-established pathogen recognition molecules such as Toll-like receptors. [source] Peptidylarginine deiminase from Porphyromonas gingivalis citrullinates human fibrinogen and ,-enolase: Implications for autoimmunity in rheumatoid arthritisARTHRITIS & RHEUMATISM, Issue 9 2010Natalia Wegner Objective To investigate protein citrullination by the periodontal pathogen Porphyromonas gingivalis as a potential mechanism for breaking tolerance to citrullinated proteins in rheumatoid arthritis (RA). Methods The expression of endogenous citrullinated proteins was analyzed by immunoblotting of cell extracts from P gingivalis and 10 other oral bacteria. P gingivalis,knockout strains lacking the bacterial peptidylarginine deiminases (PADs) or gingipains were created to assess the role of these enzymes in citrullination. Citrullination of human fibrinogen and ,-enolase by P gingivalis was studied by incubating live wild-type and knockout strains with the proteins and analyzing the products by immunoblotting and mass spectrometry. Results Endogenous protein citrullination was abundant in P gingivalis but lacking in the other oral bacteria. Deletion of the bacterial PAD gene resulted in complete abrogation of protein citrullination. Inactivation of arginine gingipains, but not lysine gingipains, led to decreased citrullination. Incubation of wild-type P gingivalis with fibrinogen or ,-enolase caused degradation of the proteins and citrullination of the resulting peptides at carboxy-terminal arginine residues, which were identified by mass spectrometry. Conclusion Our findings demonstrate that among the oral bacterial pathogens tested, P gingivalis is unique in its ability to citrullinate proteins. We further show that P gingivalis rapidly generates citrullinated host peptides by proteolytic cleavage at Arg-X peptide bonds by arginine gingipains, followed by citrullination of carboxy-terminal arginines by bacterial PAD. Our results suggest a novel model where P gingivalis,mediated citrullination of bacterial and host proteins provides a molecular mechanism for generating antigens that drive the autoimmune response in RA. [source] Gene expression signatures in chronic and aggressive periodontitis: a pilot studyEUROPEAN JOURNAL OF ORAL SCIENCES, Issue 3 2004Panos N. Papapanou This pilot study examined gene expression signatures in pathological gingival tissues of subjects with chronic or aggressive periodontitis, and explored whether new subclasses of periodontitis can be identified based on gene expression profiles. A total of 14 patients, seven with chronic and seven with aggressive periodontitis, were examined with respect to clinical periodontal status, composition of subgingival bacterial plaque assessed by checkerboard hybridizations, and levels of serum IgG antibodies to periodontal bacteria assayed by checkerboard immunoblotting. In addition, at least two pathological pockets/patient were biopsied, processed for RNA extraction, amplification and labeling, and used to study gene expression using Affymetrix U-133 A arrays. Based on a total of 35 microarrays, no significantly different gene expression profiles appeared to emerge between chronic and aggressive periodontitis. However, a de novo grouping of the 14 subjects into two fairly robust clusters was possible based on similarities in gene expression. These two groups had similar clinical periodontal status and subgingival bacterial profiles, but differed significantly with respect to serum IgG levels against the important periodontal pathogens Porphyromonas gingivalis, Tannerella forsythensis and Campylobacter rectus. These early data point to the usefulness of gene expression profiling techniques in the identification of subclasses of periodontitis with common pathobiology. [source] Antibody levels to single bacteria or in combination evaluated against myocardial infarctionJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 6 2008Lise Lund Hĺheim Abstract Background: Evidence is accumulating that oral bacteria are associated with myocardial infarctions (MI). We were interested in studying the differences in the association between single bacteria or bacteria in combination and the relation to C-reactive protein (CRP). Material and Methods: We examined the levels of antibodies against four major periodontal pathogens Porphyromonas gingivalis (PG), Aggregatibacter actinomycetemcomitans (AA), Tannerella forsythia (TF) and Treponema denticola (TD) and CRP in 548 men with a self-reported history of MI to 625 controls who took part in the Oslo II study in 2000. Results: The mean levels of bacterial antibodies were higher for the cases than the controls, but not significant as standard deviations were large. The level of CRP was higher in the cases than the controls (p=0.010). Logistic regression analyses comparing the upper quartile value with the lower value of one of either four antibodies (anti-AA, anti-TF, anti-TD and anti-PG) were significantly associated (p=0.032) with MI. Equivalent analyses of either three bacteria showed significant associations for anti-AA, anti-TD and anti-PG (p=0.036) and anti-AA, anti-PG and anti-TF (p=0.040). CRP showed an increased relative risk with increasing quartile value; trend, p=0.016, but not in multivariate analysis including the oral antigens. Conclusions: No single bacterium but rather combinations were related to increasing relative risk for MI independent of known cardiovascular risk factors. [source] | ||||||||||