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Evanthia Lalla - One of the best experts on this subject based on the ideXlab platform.
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infection with a Periodontal Pathogen increases mononuclear cell adhesion to human aortic endothelial cells
Atherosclerosis, 2007Co-Authors: Georg A Roth, Bernhard Moser, Panos N Papapanou, Ann Marie Schmidt, Franziska Rothwalter, Mary Beth Giacona, Evis Harja, Evanthia LallaAbstract:Abstract Background As a link between Periodontal infections and an increased risk for vascular disease has been demonstrated, we assessed the ability of the Gram-negative Periodontal Pathogen Porphyromonas gingivalis to modulate properties of endothelial cells linked to inflammation and proatherogenic pathways. Methods and results Primary human aortic endothelial cells (HAEC) were infected with either P. gingivalis strain 381 or its non-invasive fimbriae-deficient mutant, DPG3, and incubated with U-937 monocytes, or Jurkat T cells. P. gingivalis -infected HAEC demonstrated significantly increased adhesion of immune cells compared to non-infected cells or those infected with DPG3. Heat-killed bacteria had no effect on mononuclear cell adhesion and P. gingivalis LPS had only a minimal effect. P. gingivalis infection significantly increased HAEC expression of VCAM-1, ICAM-1 and E-selectin, and enhanced production of IL-6, IL-8 and MCP-1. Conclusion These data demonstrate that live invasive P. gingivalis 381 elicits a pro-atherogenic response in HAEC.
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infection with a Periodontal Pathogen induces procoagulant effects in human aortic endothelial cells
Journal of Thrombosis and Haemostasis, 2006Co-Authors: Georg A Roth, Bernhard Moser, S J Huang, Justin S Brandt, Y Huang, Panos N Papapanou, Ann Marie Schmidt, Evanthia LallaAbstract:Summary. Background: Multiple studies have demonstrated a link between Periodontal infections and vascular disease. Porphyromonas gingivalis, a major Periodontal Pathogen, has been shown to adhere to and invade endothelial cells. Objective: In order to dissect mechanisms underlying these observations, we assessed the role of P. gingivalis infection in modulating properties of endothelial cells linked to atherothrombosis. Methods: Primary human aortic endothelial cells (HAEC) were infected with either P. gingivalis 381 or its non-invasive fimbriae-deficient mutant, DPG3. Markers of coagulation and thrombosis were assessed 8 h and 18 h postinfection in cell lysates and supernatants. Results: Infection with P. gingivalis 381 significantly enhanced tissue factor expression and activity, and suppressed levels of tissue factor pathway inhibitor. Furthermore, P. gingivalis infection decreased levels and activity of tissue plasminogen activator, and enhanced plasminogen activator inhibitor-1 antigen and activity. Consistent with an important role for bacterial adhesion/invasion in this setting, infection with DPG3 failed to induce procoagulant properties in HAEC. Most of the above effects of P. gingivalis 381 were more apparent at the later time point (18 h postinfection). This suggests that P. gingivalis infection, rather than having an immediate and direct effect, might activate pathways that, in turn, trigger endothelial procoagulant mechanisms. Conclusions: Taken together these data demonstrate for the first time that infection with a Periodontal Pathogen induces procoagulant responses in HAEC.
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oral infection with a Periodontal Pathogen accelerates early atherosclerosis in apolipoprotein e null mice
Arteriosclerosis Thrombosis and Vascular Biology, 2003Co-Authors: Evanthia Lalla, Panos N Papapanou, Ira B Lamster, Marion A Hofmann, Loredana G Bucciarelli, Adrienne P Jerud, Sid Tucker, Ann Marie SchmidtAbstract:Objective— Because recent epidemiologic evidence suggests that Periodontal infections may increase the risk of atherosclerosis and related events in humans, we assessed the impact of oral inoculati...
Pirkko J Pussinen - One of the best experts on this subject based on the ideXlab platform.
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systemic exposure to a common Periodontal Pathogen and missing teeth are associated with metabolic syndrome
Acta Diabetologica, 2015Co-Authors: Kati Hyvarinen, Aino Salminen, Veikko Salomaa, Pirkko J PussinenAbstract:Periodontitis is a common chronic infection of tooth-supporting tissues leading to tooth loss. Two of the major Periodontal Pathogens are Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis. Clinically diagnosed periodontitis has been associated with metabolic syndrome (MetS). The aim of the study was to investigate the association of serum antibody levels against A. actinomycetemcomitans and P. gingivalis and the number of missing teeth with MetS. The population was the PAIS subcohort of the FINRISK ‘97 study (n = 1,354). The subjects were men aged 45–74 years, and they participated in this cardiovascular risk factor survey in Finland. A total of 534 (39 %) subjects had MetS defined according to the guidelines of the International Diabetes Federation. Serum antibody levels against the Pathogens were measured by multiserotype ELISA. A. actinomycetemcomitans antibody levels and the number of missing teeth were significantly higher in subjects with a large waist circumference or with low serum high-density lipoprotein cholesterol. The number of missing teeth was also higher among subjects with a high serum triglyceride concentration or high plasma glucose concentration. Seropositivity for A. actinomycetemcomitans was significantly associated with MetS with an odds ratio (OR) 1.42 (95 % confidence interval 1.09–1.85, p = 0.009). More than four missing teeth and complete edentulousness were also significantly associated with MetS with ORs 1.69 (1.26–2.27, p < 0.001) and 1.93 (1.30–2.86, p = 0.001), respectively. Missing teeth and systemic exposure to A. actinomycetemcomitans were associated with several components of Mets. Infection with this common Pathogen or the host response against it is associated with the presence of MetS.
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Periodontal Pathogen carriage rather than periodontitis determines the serum antibody levels
Journal of Clinical Periodontology, 2011Co-Authors: Pirkko J Pussinen, Eija Kononen, Susanna Paju, Kati Hyvarinen, Ulvi Kahraman Gursoy, Sisko Huumonen, Matti KnuuttilaAbstract:AIM We investigated in a nationally representative sample, how periodontitis modifies the association between the carriage of Periodontal Pathogens and serology. MATERIALS AND METHODS The population comprised 1586 dentate subjects who participated in an interview, clinical and radiological oral health examination, and saliva collection. Serum immunoglobulin A (IgA)- and IgG-class antibody levels against Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis and their salivary occurrence were determined in the whole population. The quantity of the Pathogens was measured in a subpopulation. RESULTS In the univariate analyses, the corresponding antibody levels were higher in the Pathogen carriers compared with the non-carriers, and clearly higher in the carriers with Periodontal pockets compared with the carriers without. In the multi-variate analyses, however, all antibody levels associated strongly with age (p<0.001) and the carriage of the corresponding Pathogen (p<0.001), but only weakly with the presence or number of teeth with Periodontal pockets. In the subpopulation, the antibody levels and the numbers of corresponding bacteria in saliva had a positive association, which was not affected by the disease. CONCLUSIONS The carriage of A. actinomycetemcomitans and P. gingivalis is the strongest determinant of the systemic antibody response to these Pathogens, and the extent of periodontitis has at most a modest modifying effect.
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pro atherogenic properties of lipopolysaccharide from the Periodontal Pathogen actinobacillus actinomycetemcomitans
Journal of Endotoxin Research, 2006Co-Authors: Laura Lakio, Markku Lehto, Anita M Tuomainen, Matti Jauhiainen, Ernst Malle, Sirkka Asikainen, Pirkko J PussinenAbstract:An association between cardiovascular and Periodontal disease may be due to lipopolysaccharide (LPS)-promoted release of inflammatory mediators, adverse alterations of the lipoprotein profile, and an imbalance in cholesterol homeostasis. Since periodontoPathogenic potential differs between serotypes of a major Periodontal Pathogen, Actinobacillus actinomycetemcomitans, we studied the pro-atherogenic properties of LPS preparations from serotypes b and d strains on macrophages (RAW 264.7). A. actinomycetemcomitans LPS preparations induced a time-dependent release of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). LPS induced foam cell formation and cholesteryl ester accumulation from native low density lipoprotein in the following order: A. actinomycetemcomitans strains JP2 (serotype b) > Y4 (serotype b) > IDH781 (serotype d). mRNA expression levels of scavenger receptor class B, type-I, and ATP-binding cassette transporter-1, receptors mediating cholesterol efflux from macrophages, were decreased by LPS preparations. The results suggest that the pro-atherogenic potential of A. actinomycetemcomitans LPS may depend on the infecting strain and correlate with the periodontoPathogenic potential of the Pathogen.
Norio Aoyama - One of the best experts on this subject based on the ideXlab platform.
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increased heart failure prevalence in patients with a high antibody level against Periodontal Pathogen
International Heart Journal, 2019Co-Authors: Norio Aoyama, Keitetsu Kure, Masato Minabe, Yuichi IzumiAbstract:The aim of this study was to assess whether a specific cardiovascular disease was related to an increased antibody level against a Periodontal Pathogen.A strong association between cardiovascular disease and periodontitis was shown, however, the causal relationship was not proven. Increased inflammatory reaction of patients with periodontitis was a possible factor, which connected Periodontal infection and vascular diseases.We assessed medical history, blood data, and Periodontal conditions in patients with cardiovascular diseases. Serum IgG antibody titers against major Periodontal Pathogens and existence of salivary Periodontal bacteria were analyzed.In total, 348 subjects were enrolled in this study. The patients who exhibited 10,000 counts/mL or more of salivary Porphyromonas gingivalis were divided into two groups according to the antibody level of the Pathogen. Patients with a high antibody level against Porphyromonas gingivalis exhibited a high rate of heart failure compared to the low antibody group. Mean probing pocket depth and clinical attachment level significantly increased in the high antibody group. We found that the high anti-Porphyromonas gingivalis antibody group also experienced enhanced antibody levels against other Periodontal bacteria.An increased heart failure prevalence was found in patients with a high antibody level against a major Periodontal Pathogen, Porphyromonas gingivalis.
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Toll-like receptor-2 has a critical role in Periodontal Pathogen-induced myocardial fibrosis in the pressure-overloaded murine hearts
Hypertension Research, 2017Co-Authors: Makoto Kaneko, Jun-ichi Suzuki, Norio Aoyama, Ryo Watanabe, Yuichi Izumi, Yuka Shiheido, Asuka Yoshida, Mitsuaki IsobeAbstract:Recent studies have indicated that periodontopathic bacteria might accelerate the development of cardiac fibrosis. Porphyromonas gingivalis ( P. gingivalis ), a major Periodontal bacterium, is mainly recognized by Toll-like receptor-2 (TLR-2). However, the role of TLR-2 in the acceleration of cardiac fibrosis via infections caused by Periodontal bacteria has not yet been investigated. Here we investigated the role TLR-2 has in Periodontal Pathogen-induced cardiac fibrosis. TLR-2 knockout (KO) and wild type (WT) male C57BL/6 mice were subjected to a transverse aortic constriction (TAC) surgical procedure 2 weeks after chamber implantation. After the TAC operation, mice received injections once a week of P. gingivalis or vehicle into the chambers that were implanted in the back of mice. Fractional shortening (FS) was measured using echocardiography 1 week after the TAC surgical procedure. Four weeks after the TAC surgical procedure, blood and heart samples were collected. FS in the infected group of WT mice was significantly lower than in mice that received sham operations; however, FS in the uninfected group did not decrease in a similar manner to that in the infected group. Cardiac fibrosis was significantly enhanced in TAC-operated WT mice infected with P. gingivalis ( n =14), whereas it was inhibited in TAC-operated TLR-2 KO mice infected with P. gingivalis ( n =7). The level of matrix metalloproteinase-2 (MMP-2) mRNA was higher in WT mice infected with P. gingivalis compared with non-infected WT mice. However, the level of MMP-2 mRNA was significantly lower in TLR-2 KO mice compared with that in WT mice. In conclusion, TLR-2 had a critical role in the development of cardiac fibrosis under the conditions of pressure overload and Periodontal Pathogen infection.
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a Periodontal Pathogen porphyromonas gingivalis deteriorates isoproterenol induced myocardial remodeling in mice
Hypertension Research, 2017Co-Authors: Hiroki Sato, Jun-ichi Suzuki, Norio Aoyama, Ryo Watanabe, Yuka Shiheido, Makoto Kaneko, Asuka Yoshida, Kouji Wakayama, Hidetoshi Kumagai, Yuichi IkedaAbstract:Heart failure is a serious disease induced by several conditions, including hypertrophic cardiomyopathy. Although many reports suggest that there is an association between Periodontal disease and cardiovascular disease, the mechanisms have yet to be elucidated. The purpose of this study was to clarify the relationship between Periodontal disease and heart disease, especially in cardiac hypertrophy. We used C57BL/6J mice and implanted two types of subcutaneous chambers. First, we subcutaneously implanted a coil-shaped chamber into the back of a mouse. Porphyromonas gingivalis (P.g.), a major Periodontal Pathogen, was injected into the chamber. Then, an osmotic pump was implanted to infuse isoproterenol. Four weeks after the ISO infusion, we performed echocardiography and harvested the heart and blood. We measured the serum level of anti-P.g.-IgG using ELISA. The mRNA levels of several factors were measured using PCR. We found stronger cardiomyocyte hypertrophy in the ISO(+)/P.g.(+) mice compared with the ISO(+)/P.g.(-) mice. The total square of randomly selected cardiomyocytes was 23% larger in the ISO(+)/P.g.(+) mice than in the ISO(+)/P.g.(-) mice. We detected a higher level of mRNA expression in Toll-like receptor 2 and NADPH oxidase 4 in the ISO(+)/P.g.(-) mice compared with the control group. We revealed that a Periodontal Pathogen affected ISO-induced cardiac hypertrophy via oxidative stress.
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porphyromonas gingivalis a Periodontal Pathogen enhances myocardial vulnerability thereby promoting post infarct cardiac rupture
Journal of Molecular and Cellular Cardiology, 2016Co-Authors: Yuka Shiheido, Jun-ichi Suzuki, Norio Aoyama, Ryo Watanabe, Yasuhiro Maejima, Makoto Kaneko, Kouji Wakayama, Yuichi Ikeda, Yuriko Sakamaki, Hiroshi AkazawaAbstract:There is a strong association between Periodontal disease (PD) and atherosclerosis. However, it remains unknown whether PD is also involved in myocardial damage. We hypothesized that infection with Periodontal Pathogens could cause an adverse outcome after myocardial infarction (MI). C57BL/6J mice were inoculated with Porphyromonas gingivalis (P.g.), a major Periodontal Pathogen, or injected with phosphate-buffered saline (PBS) into a subcutaneously-implanted steelcoil chamber before and after coronary artery ligation. A significant increase in mortality, due to cardiac rupture, was observed in the P.g.-inoculated MI mice. Ultrastructural examinations revealed that P.g. invaded the ischemic myocardium of the P.g.-inoculated MI mice. The expression of p18 Bax, an active form of pro-apoptotic Bax protein, markedly increased in the P.g.-inoculated MI hearts. In vitro experiments demonstrated that gingipain, a protease uniquely secreted from P.g., cleaved wild type Bax at Arg34, as evidenced by the observation that the cleavage of Bax by gingipain was completely abolished by the Arg34Ala mutation in Bax. Treatment with immunoglobulin Y against gingipain significantly decreased the mortality of the P.g.-inoculated MI mice caused by cardiac rupture. Furthermore, inoculation of P.g. also resulted in an increase of MMP-9 activity in the post-MI myocardium by enhancing oxidative stress, possibly through impairing the selective autophagy-mediated clearance of damaged mitochondria. In conclusion, infection with P.g. during MI plays a detrimental role in the healing process of the infarcted myocardium by invasion of P.g. into the myocardium, thereby promoting apoptosis and the MMP-9 activity of the myocardium, which, in turn, causes cardiac rupture.
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abstract 13014 porphyromonas gingivalis a potent Periodontal Pathogen induces cardiac rupture after myocardial infarction in mice
Circulation, 2014Co-Authors: Yuka Shiheido, Jun-ichi Suzuki, Norio Aoyama, Naho Kobayashi, Yuichi Izumi, Yasuhiro Maejima, Makoto Kaneko, Mitsuaki IsobeAbstract:Introduction: Accumulating lines of evidence suggest that there is a strong association between Periodontal disease and coronary artery diseases. However, the effects of Periodontal disease on the pathophysiology of myocardial infarction (MI) remain unknown. Hypothesis: Periodontal Pathogens mediate detrimental effects on the infarcted myocardium. Methods: C57BL/6J male mice were split into 3 groups. Before and after coronary artery ligation, each group was injected with one of the following bacteria or substance: Porphyromonas gingivalis (P.g.), Aggregatibacter actinomycetemcomitans (A.a.: a Periodontal Pathogen), or phosphate buffered saline (PBS). In vitro experiments were also conducted using cultured cardiomyocytes (CMs). Results: Observation of the mice lasted for 14 days after MI. A significant increase of mortality, due to cardiac rupture, was observed on days 4 and 5 after MI in the P.g.-injected mice compared to the A.a.-injected or PBS-injected mice (P.g. [n=19] vs PBS [n=12] 42.1 vs 0%, p < 0.05, A.a. [n=7] vs PBS [n=12] 14.2 vs 0%). The release of H2O2 from the infarcted myocardium significantly increased in the P.g. group compared to the PBS group (P.g. [n=6] vs PBS [n=6]: 31.0 ± 9.1 vs 6.3 ± 3.4 pmol, p < 0.05). In the infarcted myocardium, the protein level of matrix metalloproteinase-9 (MMP-9), a protease which interrupts the healing process of damaged tissues, was significantly accumulated in the P.g. group (3.5 ± 0.9 fold, n=7) compared to the PBS group (n=7). Zymography revealed that MMP-9 activity was significantly higher in the P.g. group (2.9 ± 0.6 fold, n=7) than in the PBS group (n=7). These results suggest that infection with P.g. promotes production of H2O2, an enhancer of the MMP-9 activity, thereby aggravating the stability of the infarcted myocardium. In addition, the level of p18 Bax, an active form of Bax that strongly promotes apoptosis, significantly increased in the P.g. group (1.7 ± 0.1 fold, n=5) compared to the PBS group (n=5). Treatment with gingipain, a cysteine protease uniquely secreted from P.g., on cultured CMs promoted the accumulation of p18 Bax and CMs death. Conclusions: Infection with P.g. during MI plays a detrimental role in the healing process of the myocardium, which in turn contributes to cardiac rupture.
Graham P Stafford - One of the best experts on this subject based on the ideXlab platform.
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Periodontal Pathogen sialometabolic activity in periodontitis
2020Co-Authors: Graham P Stafford, Ashu SharmaAbstract:Periodontitis is a common bacterially induced inflammatory condition that damages the tooth-supporting apparatus and negatively impacts the systemic health. It affects over 700 million people worldwide with an estimated economic burden totaling to $442 billion annually. A bacterial triad in the subgingival niche comprising of Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia is very influential in the development of periodontitis. Significantly, all these three Pathogens produce a sialidase enzyme that can cleave terminal sialic acid residue from host-derived sialoglycoproteins, such as present on the surface of oral epithelial cells and in saliva and gingival crevicular fluid. This ability to release and utilize sialic acid from host glycoproteins is crucial for their growth and immune evasion and survival strategies. In addition, sialic acid cleavage can cause immune dysfunction and disruption of tissue integrity and thus exacerbate Periodontal inflammation in various ways. Here, we propose that inhibition of Pathogen-derived sialidase activity with sialidase-targeting pharmacological drugs may be an attractive adjunct therapy in the treatment of periodontitis.
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Periodontal Pathogen cazymes host Pathogen biology biochemistry and biotechnological exploitation
Journal of Oral Microbiology, 2017Co-Authors: Graham P Stafford, Andrew M Frey, Marianne J SaturAbstract:One often neglected aspect of the host-Pathogen interface is the presence of myriad glycoproteins and the carbohydrate glycans that they present. These are often the first point of contact for bact...
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characterization of an α l fucosidase from the Periodontal Pathogen tannerella forsythia
Virulence, 2015Co-Authors: Zoe Anne Megson, Andrea Koerdt, Bettina Janesch, Kathryn L Naylor, I B H Wilson, Graham P Stafford, Andrew M Frey, H. Schuster, Roland Ludwig, Paul MessnerAbstract:The Periodontal Pathogen Tannerella forsythia expresses several glycosidases which are linked to specific growth requirements and are involved in the invasion of host tissues. α-l-Fucosyl residues are exposed on various host glycoconjugates and, thus, the α-l-fucosidases predicted in the T. forsythia ATCC 43037 genome could potentially serve roles in host-Pathogen interactions. We describe the molecular cloning and characterization of the putative fucosidase TfFuc1 (encoded by the bfo_2737 = Tffuc1 gene), previously reported to be present in an outer membrane preparation. In terms of sequence, this 51-kDa protein is a member of the glycosyl hydrolase family GH29. Using an artificial substrate, p-nitrophenyl-α-fucose (KM 670 μM), the enzyme was determined to have a pH optimum of 9.0 and to be competitively inhibited by fucose and deoxyfuconojirimycin. TfFuc1 was shown here to be a unique α(1,2)-fucosidase that also possesses α(1,6) specificity on small unbranched substrates. It is active on mucin after sia...
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characterization of an α l fucosidase from the Periodontal Pathogen tannerella forsythia
Virulence, 2015Co-Authors: Zoe Anne Megson, Andrea Koerdt, Bettina Janesch, Kathryn L Naylor, I B H Wilson, Graham P Stafford, Andrew M Frey, H. Schuster, Roland Ludwig, Paul MessnerAbstract:The Periodontal Pathogen Tannerella forsythia expresses several glycosidases which are linked to specific growth requirements and are involved in the invasion of host tissues. α-l-Fucosyl residues are exposed on various host glycoconjugates and, thus, the α-l-fucosidases predicted in the T. forsythia ATCC 43037 genome could potentially serve roles in host-Pathogen interactions. We describe the molecular cloning and characterization of the putative fucosidase TfFuc1 (encoded by the bfo_2737 = Tffuc1 gene), previously reported to be present in an outer membrane preparation. In terms of sequence, this 51-kDa protein is a member of the glycosyl hydrolase family GH29. Using an artificial substrate, p-nitrophenyl-α-fucose (KM 670 μM), the enzyme was determined to have a pH optimum of 9.0 and to be competitively inhibited by fucose and deoxyfuconojirimycin. TfFuc1 was shown here to be a unique α(1,2)-fucosidase that also possesses α(1,6) specificity on small unbranched substrates. It is active on mucin after sialidase-catalyzed removal of terminal sialic acid residues and also removes fucose from blood group H. Following knock-out of the Tffuc1 gene and analyzing biofilm formation and cell invasion/adhesion of the mutant in comparison to the wild-type, it is most likely that the enzyme does not act extracellularly. Biochemically interesting as the first fucosidase in T. forsythia to be characterized, the biological role of TfFuc1 may well be in the metabolism of short oligosaccharides in the periplasm, thereby indirectly contributing to the virulence of this organism. TfFuc1 is the first glycosyl hydrolase in the GH29 family reported to be a specific α(1,2)-fucosidase.
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a quantitative proteomic analysis of biofilm adaptation by the Periodontal Pathogen tannerella forsythia
Proteomics, 2010Co-Authors: Trong Khoa Pham, Josselin Noirel, Phillip C. Wright, Ian Douglas, Graham P StaffordAbstract:Tannerella forsythia is a Gram-negative anaerobe that is one of the most prominent inhabitants of the sub-gingival plaque biofilm, which is crucial for causing periodontitis. We have used iTRAQ proteomics to identify and quantify alterations in global protein expression of T. forsythia during growth in a biofilm. This is the first proteomic study concentrating on biofilm growth in this key Periodontal Pathogen, and this study has identified several changes in protein expression. Moreover, we introduce a rigorous statistical method utilising peptide-level intensities of iTRAQ reporters to determine which proteins are significantly regulated. In total, 348 proteins were identified and quantified with the expression of 44 proteins being significantly altered between biofilm and planktonic cells. We identified proteins from all cell compartments, and highlighted a marked upregulation in the relative abundances of predicted outer membrane proteins in biofilm cells. These included putative transport systems and the T. forsythia S-layer proteins. These data and our finding that the butyrate production pathway is markedly downregulated in biofilms indicate possible alterations in host interaction capability. We also identified upregulation of putative oxidative stress response proteins, and showed that biofilm cells are 10 to 20 fold more resistant to oxidative stress. This may represent an important adaptation of this organism to prolonged persistence and immune evasion in the oral cavity.
Tomohisa Nezu - One of the best experts on this subject based on the ideXlab platform.
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abstract wp209 serum anti Periodontal Pathogen antibody associated with atrial fibrillation and carotid plaque
Stroke, 2013Co-Authors: Naohisa Hosomi, Shiro Aoki, Tomohisa Nezu, Toshiho Ohtsuki, Takemori Yamawaki, Masayasu MatsumotoAbstract:Background: We evaluated whether serum antibody levels against individual Periodontal Pathogens are significantly associated with ischemic stroke subtypes and their risk factors. Methods: Patients with acute ischemic stroke (n=132; 74 male and 58 female, 71.3±10.7 years) and patients with no previous stroke (n=77; 38 male and 39 female, 70.7±9.5 years) were consecutively enrolled in this study. Stroke subtype was evaluated based on the TOAST classification. Serum was obtained from each patient after obtaining the patient’s consent to participate in this study. The levels of serum antibodies against Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), and Prevotella intermedia (Pi) were evaluated by ELISA. Results: The serum-antibody level of Pi was significantly higher in atherothrombotic-stroke patients than in patients with no previous stroke (p Conclusions: Our results suggest that anti-Pg antibody is associated with atrial fibrillation and anti-Pi antibody is associated with carotid artery atherosclerosis. Additionally, anti-Pi antibody may be associated with atherothrombotic stroke through its association with carotid artery atherosclerosis.
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association of serum anti Periodontal Pathogen antibody with ischemic stroke
Cerebrovascular Diseases, 2012Co-Authors: Naohisa Hosomi, Shiro Aoki, Katsuhiko Matsuo, Kazushi Deguchi, Hisashi Masugata, Koji Murao, Noriko Ichihara, Hideo Ohyama, Hiroaki Dobashi, Tomohisa NezuAbstract:Background: Periodontitis increases the risk of atherosclerotic cardiovascular disease and ischemic stroke. In this study, we evaluated whether serum antibody levels against individual Periodontal Pathogens are significantly associated with ischemic stroke subtypes and their risk factors. Methods: Patients with acute ischemic stroke (n = 132; 74 male and 58 female, 71.3 ± 10.7 years) and patients with no previous stroke (n = 77; 38 male and 39 female, 70.7 ± 9.5 years) were consecutively enrolled in this study. Stroke subtype was evaluated based on the Trial of Org 10172 in Acute Stroke Treatment classification. Serum was obtained from each patient after obtaining their consent to participate in the study. The levels of serum antibodies against Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg) and Prevotella intermedia (Pi) were evaluated by ELISA. Serum high-sensitivity C-reactive protein (hs-CRP) levels were measured by nephelometry. Results: Serum hs-CRP levels were significantly associated with acute ischemic stroke even after controlling for acute ischemic stroke, hypertension, diabetes mellitus and bulb/ internal carotid artery (ICA) atherosclerosis which were statistically selected (coefficient 0.245, 95% CI 0.142–0.347, p 2 = 35.5, R2 = 0.18, n = 209, p 2 = 46.1, R2 = 0.18, n = 209, p 2 = 77.0, R2 = 0.44, n = 129, p 2 = 98.0, R2 = 0.56, n = 129, p Conclusions: Our results suggest that anti-Pg antibody is associated with atrial fibrillation and that anti-Pi antibody is associated with carotid artery atherosclerosis. In addition, anti-Pi antibody may be associated with atherothrombotic stroke through its association with carotid artery atherosclerosis. Thus, periodontitis may lead to serious systemic diseases.
