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9
Porphyromonas gingivalis-host interactions in a Drosophila melanogaster model.牙龈卟啉单胞菌与果蝇模型中的宿主相互作用。
Infect Immun. 2011 Jan;79(1):449-58. doi: 10.1128/IAI.00785-10. Epub 2010 Nov 1.

本文引用的文献

1
Porphyromonas gingivalis-host interactions in a Drosophila melanogaster model.牙龈卟啉单胞菌与果蝇模型中的宿主相互作用。
Infect Immun. 2011 Jan;79(1):449-58. doi: 10.1128/IAI.00785-10. Epub 2010 Nov 1.
2
Porphyromonas gingivalis induce apoptosis in human gingival epithelial cells through a gingipain-dependent mechanism.牙龈卟啉单胞菌通过一种依赖牙龈蛋白酶的机制诱导人牙龈上皮细胞凋亡。
BMC Microbiol. 2009 May 27;9:107. doi: 10.1186/1471-2180-9-107.
3
Gingipains from Porphyromonas gingivalis synergistically induce the production of proinflammatory cytokines through protease-activated receptors with Toll-like receptor and NOD1/2 ligands in human monocytic cells.牙龈卟啉单胞菌的牙龈蛋白酶通过蛋白酶激活受体与Toll样受体以及人单核细胞中的NOD1/2配体协同诱导促炎细胞因子的产生。
Cell Microbiol. 2008 May;10(5):1181-9. doi: 10.1111/j.1462-5822.2008.01119.x. Epub 2008 Jan 7.
4
Involvement of minor components associated with the FimA fimbriae of Porphyromonas gingivalis in adhesive functions.牙龈卟啉单胞菌FimA菌毛相关次要成分在黏附功能中的作用
Microbiology (Reading). 2007 Jun;153(Pt 6):1916-1925. doi: 10.1099/mic.0.2006/005561-0.
5
Drosophila eiger mutants are sensitive to extracellular pathogens.果蝇艾格突变体对细胞外病原体敏感。
PLoS Pathog. 2007 Mar;3(3):e41. doi: 10.1371/journal.ppat.0030041.
6
The host defense of Drosophila melanogaster.黑腹果蝇的宿主防御。
Annu Rev Immunol. 2007;25:697-743. doi: 10.1146/annurev.immunol.25.022106.141615.
7
A systems biology analysis of the Drosophila phagosome.果蝇吞噬体的系统生物学分析
Nature. 2007 Jan 4;445(7123):95-101. doi: 10.1038/nature05380. Epub 2006 Dec 6.
8
Cutting Edge: TLR2 is required for the innate response to Porphyromonas gingivalis: activation leads to bacterial persistence and TLR2 deficiency attenuates induced alveolar bone resorption.前沿:牙龈卟啉单胞菌的固有免疫反应需要TLR2:激活导致细菌持续存在,而TLR2缺陷可减轻诱导的牙槽骨吸收。
J Immunol. 2006 Dec 15;177(12):8296-300. doi: 10.4049/jimmunol.177.12.8296.
9
Porphyromonas gingivalis minor fimbriae are required for cell-cell interactions.牙龈卟啉单胞菌的微小菌毛是细胞间相互作用所必需的。
Infect Immun. 2006 Oct;74(10):6011-5. doi: 10.1128/IAI.00797-06.
10
The nitric oxide scavenger cobinamide profoundly improves survival in a Drosophila melanogaster model of bacterial sepsis.一氧化氮清除剂钴胺酰胺可显著提高果蝇细菌性败血症模型的存活率。
FASEB J. 2006 Sep;20(11):1865-73. doi: 10.1096/fj.06-5780com.

牙龈卟啉单胞菌在果蝇模型中的毒力。

Porphyromonas gingivalis virulence in a Drosophila melanogaster model.

机构信息

Section of Oral Biology, College of Dentistry, The Ohio State University, 3185 Postle Hall, 305 W. Twelfth Avenue, Columbus, OH 43210, USA.

出版信息

Infect Immun. 2011 Jan;79(1):439-48. doi: 10.1128/IAI.00784-10. Epub 2010 Nov 1.

DOI:10.1128/IAI.00784-10
PMID:21041487
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3019912/
Abstract

Porphyromonas gingivalis has been implicated in the etiology of adult periodontitis. In this study, we examined the viability of Drosophila melanogaster as a new model for examining P. gingivalis-host interactions. P. gingivalis (W83) infection of Drosophila resulted in a systemic infection that killed in a dose-dependent manner. Differences in the virulence of several clinically prevalent P. gingivalis strains were observed in the Drosophila killing model, and the results correlated well with studies in mammalian infection models and human epidemiologic studies. P. gingivalis pathobiology in Drosophila did not result from uncontrolled growth of the bacterium in the Drosophila hemolymph (blood) or overt damage to Drosophila tissues. P. gingivalis killing of Drosophila was multifactorial, involving several bacterial factors that are also involved in virulence in mammals. The results from this study suggest that many aspects of P. gingivalis pathogenesis in mammals are conserved in Drosophila, and thus the Drosophila killing model should be useful for characterizing P. gingivalis-host interactions and, potentially, polymicrobe-host interactions.

摘要

牙龈卟啉单胞菌与成人牙周炎的病因有关。在这项研究中,我们研究了黑腹果蝇作为研究牙龈卟啉单胞菌-宿主相互作用的新模型的可行性。牙龈卟啉单胞菌(W83)感染果蝇导致全身性感染,且呈剂量依赖性致死。在果蝇杀伤模型中观察到几种临床常见牙龈卟啉单胞菌菌株的毒力差异,其结果与哺乳动物感染模型和人类流行病学研究的结果非常吻合。在果蝇中,牙龈卟啉单胞菌的病理生物学不是由其在果蝇血淋巴(血液)中的不受控制生长或对果蝇组织的明显损伤引起的。牙龈卟啉单胞菌杀伤果蝇是多因素的,涉及到几种也与哺乳动物毒力有关的细菌因子。这项研究的结果表明,哺乳动物中许多牙龈卟啉单胞菌发病机制的方面在果蝇中是保守的,因此,果蝇杀伤模型应该有助于表征牙龈卟啉单胞菌-宿主相互作用,并且可能有助于多微生物-宿主相互作用。