牙龈卟啉单胞菌与病毒的交互作用

慢性牙周炎是人类最常见的口腔疾病之一,目前其公认的主要致病菌为牙龈卟啉单胞菌。在牙周病位点中可检测到多种病毒株,病毒和细菌病原体联合作用的感染机制复杂,牙龈卟啉单胞菌与多种病毒有交互作用的特性,牙周病的迁延不愈以及与多种系统性疾病相关的特性可能与此相关。本研究就牙龈卟啉单胞菌对病毒相关性疾病的促进作用作一综述,以期为牙周病连同病毒性疾病感染患者的治疗提供新思路。     

牙龈卟啉单胞菌与动脉粥样硬化发病的关系

慢性牙周炎是心血管疾病特别是冠心病的危险因素之一,然而其相关的生物学基础目前尚不清楚.笔者下面就与慢性牙周炎关系最为密切的牙龈卟啉单胞菌与动脉粥样硬化的相关性和牙龈卟啉单胞菌致动脉粥样硬化的可能机制以及Toll样受体在牙龈卟啉单胞菌与动脉粥样硬化相关性中的作用作一综述.     

抗牙龈卟啉单胞菌IgY的制备及抑菌效果

目的:使用牙龈卟啉单胞菌(P.g)诱导产蛋母鸡特异性IgY抗体产生及制备,特异性IgY抗体抑制P.g及其它牙周病病因菌生长.方法:采用免疫接种、水稀释、盐析、液体培养抑菌及ELISA等方法,诱导、提纯IgY抗体,抑制P.g及其它牙周病病因菌生长.结果:诱导产生的IgY抗体经硫酸铵盐析提取纯度达87.6%～89.1%,IgY特异性结合牙龈卟啉单胞菌抗原的结合效价1∶ 1 600.制备的抗牙龈卟啉单胞菌IgY抗体与牙龈二氧化碳噬纤维菌、中间普氏菌、伴放线放线杆菌、具核梭杆菌等牙周病致病菌的交叉免疫反应抗原结合效价分别为1∶ 800、1∶ 800、1∶ 6 400、1∶ 12 800.抗牙龈卟啉单胞菌IgY在5.0、1.0、0.1 g/L时,分别与牙龈卟啉单胞菌、牙龈二氧化碳噬纤维菌、伴放线放线杆菌、中间普氏菌、具核梭杆菌、粘性放线菌、变形链球菌等厌氧菌在(1×108) CFU/L和(5×108) CFU/L时培养24 h和72 h均有不同程度的抑制其生长作用.结论:牙龈卟啉单胞菌免疫产蛋母鸡诱导产生的特异性IgY抗体在一定的浓度内有抑制牙龈卟啉单胞菌生长,以及抑制多种牙周病致病菌生长的作用.牙龈卟啉单胞菌与这些牙周病病因均存在着共同抗原,其可能具有防治牙周病的前景.     

牙龈卟啉单胞菌对铁和亚铁血红素的摄取机制

牙龈卟啉单胞菌(Porphyromonas gingivalis,P.g)是慢性牙周病重要病原菌之一.作为绝对需铁菌,牙龈卟啉单胞菌不能产生铁载体.所以在人体中,牙龈卟啉单胞菌主要利用外源的铁/亚铁血红素,通过特异性外膜受体结合含铁蛋白中的铁/亚铁血红素,并将其转运至细胞内.铁/亚铁血红素对于牙龈卟啉单胞菌的生长和毒性都起着重要作用.本文主要介绍牙龈卟啉单胞菌对铁和亚铁血红素的摄取机制.     

牙龈卟啉单胞菌与冠心病之间的关系

牙龈卟啉单胞菌既是牙周病主要的可疑致病菌，亦是冠心病潜在的危险因素，因此牙周病是否为引起冠心病的危险因素之一引起了诸多研究者的兴趣。本文就牙龈卟啉单胞菌，牙龈卟啉单胞菌可能引起冠心病的致病过程和机制等研究进展作一综述。     

牙龈卟啉单胞菌对不同组织来源血管内皮 细胞的作用及机制的研究进展

牙龈卟啉单胞菌是重要的牙周可疑致病菌。牙龈卟啉单胞菌可黏附、侵入并损伤血管内皮细胞,并进入远隔组织器官内,以此参与动脉粥样硬化、阿尔兹海默病等全身疾病的发生和发展过程。近年来研究发现牙龈卟啉单胞菌对不同组织来源血管内皮细胞的致病性及其作用机制均有不同。本文就牙龈卟啉单胞菌对不同组织来源血管内皮细胞的作用及机制作一综述,以拓宽牙龈卟啉单胞菌与全身性疾病的研究思路。     

牙龈卟啉单胞菌在牙周病防治中的应用

牙周病是口腔两大类主要疾病之一,具有较高的发病率,因此,探索预防牙周病的有效途径十分重要。本文介绍了国外学者以牙龈卟啉单胞菌不同形式的抗原进行免疫学防治牙周炎的试验,其中包括对牙龈卟啉单胞菌菌毛、血凝素、牙龈素和外膜蛋白的研究。     

薄荷复方煎液对龋病、牙周病致病菌杀菌作用的研究

目的：研究薄荷复方煎液对龋病、牙周病致病菌的抑制和杀灭作用。方法：致龋菌血链球菌、变形链球菌和牙周病致病菌牙龈卟啉单胞菌分离培养,将薄荷复方煎液配成不同浓度,分别对4种细菌做药敏试验,记录各自的最小抑菌浓度（MIC）和最小杀菌浓度（MBC）。结果：血链球菌MIC1：32,变形链球菌MIC1：4,牙龈卟啉单胞菌MIC1：32;血链球菌MBC1：16,变形链球菌MBC1：1,牙龈卟啉单胞菌MBC1：8。结论：薄荷复方煎液对龋病、牙周病致病菌有抑制和杀灭作用。     

牙龈卟啉单胞菌膜泡对牙龈上皮细胞MMPs基因表达的影响

目的:探讨牙龈卟啉单胞菌膜泡对牙龈上皮细胞基质金属蛋白酶(MMPs)基因表达的影响,揭示牙龈卟啉单胞菌在牙周炎中的致病作用.方法:以Real-time RT-PCR法检测牙龈卟啉单胞菌膜泡刺激下牙龈上皮细胞MMP-1和MMP-3的mRNA表达水平.结果:牙龈卟啉单胞菌膜泡显著地上调MMP-1和MMP-3 mRNA表达水平.结论:牙龈卟啉单胞菌诱导牙龈上皮细胞发生细胞炎症反应,可能是牙周炎发生、发展的重要因素.     

牙龈卟啉单胞菌研究进展

牙周炎是常见的口腔疾病之一,是中国成年人失牙的主要原因.牙龈卟啉单胞菌在引发牙周组织破坏过程中发挥着重要的作用,成为国内外学者研究的热点之一.本文就牙龈卟啉单胞菌与口腔疾病和其他全身性疾病的关系、牙龈卟啉单胞菌全基因组,牙龈卟啉单胞菌与牙龈上皮细胞的相互作用等研究作一综述,以拓宽牙龈卟啉单胞菌的研究思路,进血为牙周炎的...     

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??Phenotypic alteration??proliferation??migration??calcification and other biological activity changes may occur in vascular smooth muscle cells??which have an important impact on the development of atherosclerosis??AS??. Epidemiological surveys and experiments in vivo and in vitro have demonstrated that periodontitis is closely related to AS. Porphyromonas gingivalis ??P·gingivalis?? is recognized as one of the major pathogens of chronic periodontitis. The P·gingivalis promotes atherosclerosis formation by way of penetrating through the interior of the cells??changing the structure of cells??stimulating proliferation and migration??and promoting inflammatory cytokines secretion and calcification. This article reviews the biological activities of VSMCs influenced by P·gingivalis in order to reveal the connection between periodontitis and atherosclerosis and provide some ideas for researches.     

Biological foundation for periodontitis as a potential risk factor for atherosclerosis

OBJECTIVES: Links between periodontal diseases and systemic diseases have been well documented by epidemiological studies. Recently, research has shifted to elucidating the biologic mechanism for a causal relationship. One focus of interest is atherosclerosis, the underlying event of cardiovascular diseases due to its serious health impact. However, it is still not clear whether periodontopathic pathogens are truly etiologic agents or ubiquitous bystanders. This article reviews the current understanding about the molecular biological interactions between periodontal disease and atherosclerosis and the biological plausibility of periodontitis as a potential risk factor for cardiovascular disease. MATERIALS AND METHODS: The current literature regarding periodontal diseases and atherosclerosis and coronary vascular disease was searched using the Medline and PubMed databases. RESULTS: In vitro experiments and animal models are appropriate tools to investigate the biological interactions between periodontal disease and atherosclerosis at the cell molecular level. The concepts linking both pathologies refer to inflammatory response, immune responses, and hemostasis. In particular, Porphyromonas gingivalis appears to have unique, versatile pathogenic properties. Whether or not these findings from isolated cells or animal models are applicable in humans with genetic and environmental variations is yet to be determined. Likewise, the benefit from periodontal therapy on the development of atherosclerosis is unclear. Approaches targeting inflammatory and immune responses of periodontitis and atherosclerosis simultaneously are very intriguing. CONCLUSION: An emerging concept suggests that a pathogenic burden from different sources might overcome an individual threshold culminating in clinical sequela. P. gingivalis contributes directly and indirectly to atherosclerosis.     

Anti-P. gingivalis response correlates with atherosclerosis

Significant associations between atherosclerosis and both Porphyromonas gingivalis, a major periodontopathogen, and the respiratory pathogen, Chlamydia pneumoniae, have been shown. Many individuals with evidence of atherosclerosis demonstrate seropositivity to these pathogens. The aim of the present study was to examine the atherogenic effect of repeated immunizations with either or both of these agents, and to determine if molecular mimicry of bacterial heat-shock protein (HSP), termed GroEL, and host (h) HSP60 was involved. Atherogenesis was examined in apolipoprotein-E-deficient (-/-) mice following intraperitoneal immunizations with P. gingivalis, C. pneumoniae, P. gingivalis, and C. pneumoniae or vehicle. Lesion area in the proximal aorta and levels of serum antibodies to P. gingivalis, C. pneumoniae, and GroEL were measured. The increased pathogen burden of P. gingivalis, but not of C. pneumoniae, enhanced atherosclerosis. hHSP60 was detected in lesions, and in P. gingivalis-immunized mice, lesion development was correlated with anti-GroEL antibody levels, supporting the involvement of molecular mimicry between GroEL and hHSP60.     

Epitope mapping of Porphyromonas gingivalis heat-shock protein and human heat-shock protein in human atherosclerosis

To identify T- and/or cross-reactive B-cell epitopes of P. gingivalis and human heat-shock protein (HSP)60 in atherosclerosis patients, we synthesized 104 overlapping synthetic peptides spanning whole molecules of P. gingivalis HSP60 and human HSP60, respectively. T-cell epitopes of P. gingivalis HSP were identified with the use of previously established P. gingivalis HSP-reactive T-cell lines. B-cell epitopes of P. gingivalis HSP60 and human HSP60 were identified by the use of patients' sera. Anti-P. gingivalis, anti-P. gingivalis HSP60, or anti-human HSP60 IgG antibody titers were higher in the atherosclerosis patients compared with the healthy subjects. Five immunodominant peptides of P. gingivalis HSP60, identified as T-cell epitopes, were also found to be B-cell epitopes. Moreover, 6 cross-reactive B-cell epitopes of human HSP60 were identified. It was concluded that P. gingivalis HSP60 might be involved in the immunoregulatory process of atherosclerosis, with common T- and/or B-cell epitope specificities and with cross-reactivity with human HSP60.     

Immune responses to heat shock protein in Porphyromonas gingivalis-infected periodontitis and atherosclerosis patients

BACKGROUND: It has been widely thought that heat shock protein might be involved in autoimmune disease mechanisms in humans. OBJECTIVES: The present study was performed to evaluate the recognition of Porphyromonas gingivalis heat shock protein 60 (hsp60) and human hsp60 by immune sera in P. gingivalis-infected periodontitis and atherosclerosis patients. MATERIALS AND METHODS: Mononuclear cells from atheroma lesions were stimulated with P. gingivalis hsp and sera from periodontitis or atherosclerosis patients were subjected to Western immunoblotting to P. gingivalis hsp or human hsp, respectively. RESULTS: Western immunoblot analysis demonstrated the dual reactivity of anti-P. gingivalis antisera with P. gingivalis hsp and human hsp. We could also establish P. gingivalis hsp-specific T cell lines from the atheroma lesions, a mixture of CD4+ and CD8+ cells producing the cytokines characteristic of both Th1 and Th2 subsets. CONCLUSION: These observations suggest the modulating effect of P. gingivalis hsp60 in the immunopathogenesis of periodontitis and atherosclerosis.     

T-cell clonality to Porphyromonas gingivalis and human heat shock protein 60s in patients with atherosclerosis and periodontitis

Individuals with periodontitis have been reported to have a significantly increased risk of developing coronary heart disease. Several studies have demonstrated that the immune response to heat shock protein 60 (HSP60) may be involved in the pathogenesis of both atherosclerosis and chronic periodontitis. To investigate this possible link between these diseases, cellular and humoral immune responses to HSP60 in atherosclerosis patients were compared with those in periodontitis patients and healthy subjects using human and Porphyromonas gingivalis HSP60 (GroEL) as antigens. Antibody levels to both human and P. gingivalis HSP60s were the highest in atherosclerosis patients, followed by periodontitis patients and healthy subjects. Clonal analysis of the T cells clearly demonstrated the presence of not only human HSP60- but also P. gingivalis GroEL-reactive T-cell populations in the peripheral circulation of atherosclerosis patients. Furthermore, these HSP60-reactive T cells seemed to be present in atherosclerotic lesions in some patients. These results suggest that T-cell clones with the same specificity may be involved in the pathogenesis of the different diseases.     

Cross-reactivity of GroEL antibodies with human heat shock protein 60 and quantification of pathogens in atherosclerosis

BACKGROUND/AIMS: Chronic infections such as those caused by Chlamydia pneumoniae and periodontopathic bacteria such as Porphyromonas gingivalis have been associated with atherosclerosis, possibly due to cross-reactivity of the immune response to bacterial GroEL with human heat shock protein (hHSP) 60. METHODS: We examined the cross-reactivity of anti-GroEL and anti-P. gingivalis antibodies with hHSP60 in atherosclerosis patients and quantified a panel of six pathogens in atheromas. RESULTS: After absorption of plasma samples with hHSP60, there were variable reductions in the levels of anti-GroEL and anti-P. gingivalis antibodies, suggesting that these antibodies cross-reacted with hHSP60. All of the artery specimens were positive for P. gingivalis. Fusobacterium nucleatum, Tannerella forsythia, C. pneumoniae, Helicobacter pylori, and Haemophilus influenzae were found in 84%, 48%, 28%, 4%, and 4% of arteries, respectively. The prevalence of the three periodontopathic microorganisms, P. gingivalis, F. nucleatum and T. forsythia, was significantly higher than that of the remaining three microorganisms. CONCLUSIONS: These results support the hypothesis that in some patients, cross-reactivity of the immune response to bacterial HSPs including those of periodontal pathogens, with arterial endothelial cells expressing hHSP60 may be a possible mechanism for the association between atherosclerosis and periodontal infection.