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本文引用的文献

1
Treponema denticola activates mitogen-activated protein kinase signal pathways through Toll-like receptor 2.齿垢密螺旋体通过Toll样受体2激活丝裂原活化蛋白激酶信号通路。
Infect Immun. 2007 Dec;75(12):5763-8. doi: 10.1128/IAI.01117-07. Epub 2007 Oct 8.
2
The major outer sheath protein of Treponema denticola selectively inhibits Rac1 activation in murine neutrophils.齿垢密螺旋体的主要外鞘蛋白可选择性抑制小鼠中性粒细胞中的Rac1激活。
Cell Microbiol. 2008 Feb;10(2):344-54. doi: 10.1111/j.1462-5822.2007.01045.x. Epub 2007 Sep 13.
3
Treponema denticola in disseminating endodontic infections.具核梭杆菌在播散性牙髓感染中的作用
J Dent Res. 2006 Aug;85(8):761-5. doi: 10.1177/154405910608500814.
4
Treponema denticola infection is not a cause of false positive Treponema pallidum serology.齿垢密螺旋体感染不是梅毒螺旋体血清学假阳性的原因。
New Microbiol. 2005 Jul;28(3):215-21.
5
Detection of bacteria in endodontic samples by polymerase chain reaction assays and association with defined clinical signs in Italian patients.通过聚合酶链反应分析检测意大利患者牙髓样本中的细菌及其与特定临床症状的关联。
Oral Microbiol Immunol. 2005 Oct;20(5):289-95. doi: 10.1111/j.1399-302X.2005.00227.x.
6
Immunological evaluation and cellular location analysis of the TprI antigen of Treponema pallidum subsp. pallidum.梅毒螺旋体苍白亚种TprI抗原的免疫学评估及细胞定位分析
Infect Immun. 2005 Jun;73(6):3817-22. doi: 10.1128/IAI.73.6.3817-3822.2005.
7
Spirochetes at the forefront of periodontal infections.处于牙周感染前沿的螺旋体。
Periodontol 2000. 2005;38:13-32. doi: 10.1111/j.1600-0757.2005.00108.x.
8
Molecular detection of Treponema denticola and Porphyromonas gingivalis in carotid and aortic atheromatous plaques by FISH: report of two cases.通过荧光原位杂交技术对颈动脉和主动脉粥样斑块中齿垢密螺旋体和牙龈卟啉单胞菌进行分子检测:两例报告
J Med Microbiol. 2005 Jan;54(Pt 1):93-96. doi: 10.1099/jmm.0.45845-0.
9
Intraoral dissemination of treponemes after periodontal therapy.牙周治疗后口腔内梅毒螺旋体的传播。
Clin Oral Investig. 2004 Dec;8(4):219-25. doi: 10.1007/s00784-004-0272-5. Epub 2004 Jun 23.
10
The periplasmic flagellum of spirochetes.螺旋体的周质鞭毛。
J Mol Microbiol Biotechnol. 2004;7(1-2):30-40. doi: 10.1159/000077867.

鼠腹腔巨噬细胞杀伤密螺旋体。

Killing of Treponema denticola by mouse peritoneal macrophages.

机构信息

Department of Haematology and Oncology L. and A. Seragnoli, Section of Microbiology, University of Bologna, St. Orsola Hospital, 9 via G. Massarenti, 40138 Bologna, Italy.

出版信息

J Dent Res. 2010 May;89(5):521-6. doi: 10.1177/0022034510363105. Epub 2010 Mar 3.

DOI:10.1177/0022034510363105
PMID:20200417
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2868591/
Abstract

Treponema denticola has been identified as an important cause of periodontal disease and hypothesized to be involved in extra-oral infections. The objective of this study was to investigate the role of T. denticola cell length and motility during mouse peritoneal macrophages in vitro uptake. Macrophages, incubated under aerobic and anaerobic conditions, produced a similar amount of TNF-alpha when stimulated with Escherichia coli LPS. The uptake of FlgE- and CfpA-deficient mutants of T. denticola was significantly increased compared with the wild-type strain, due to cell size or lack of motility. Opsonization with specific antibodies considerably improved the treponemes' uptake. These results suggest that macrophages, in addition to other phagocytes, could play an important role in the control of T. denticola infection, and that the raising of specific antibodies could improve the efficacy of the immune response toward T. denticola, either at an oral site or during dissemination.

摘要

齿密螺旋体已被确定为牙周病的重要病因,并被假设与口腔外感染有关。本研究的目的是研究齿密螺旋体细胞长度和运动性在体外摄取小鼠腹腔巨噬细胞中的作用。在需氧和厌氧条件下孵育的巨噬细胞,在受到大肠杆菌 LPS 刺激时产生相似量的 TNF-α。与野生型菌株相比,FlgE- 和 CfpA 缺陷突变体的摄取明显增加,这归因于细胞大小或缺乏运动性。用特异性抗体调理显著提高了密螺旋体的摄取。这些结果表明,巨噬细胞除其他吞噬细胞外,可能在控制密螺旋体感染方面发挥重要作用,并且特异性抗体的产生可提高针对密螺旋体的免疫反应的效果,无论是在口腔部位还是在传播过程中。