• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

What is the relevance of lung epithelial cells during the dissemination of spores in inhalational anthrax?

作者信息

Tournier Jean-Nicolas, Cleret Aurélie, Quesnel-Hellmann Anne

出版信息

Infect Immun. 2009 Jan;77(1):565; author reply 565-6. doi: 10.1128/IAI.01160-08.

DOI:10.1128/IAI.01160-08
PMID:19098284
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2612284/
Abstract
摘要

相似文献

1
What is the relevance of lung epithelial cells during the dissemination of spores in inhalational anthrax?在吸入性炭疽中,肺上皮细胞在孢子传播过程中起什么作用?
Infect Immun. 2009 Jan;77(1):565; author reply 565-6. doi: 10.1128/IAI.01160-08.
2
Updating perspectives on the initiation of Bacillus anthracis growth and dissemination through its host.更新对炭疽杆菌在宿主中生长和传播的启动的观点。
Infect Immun. 2012 May;80(5):1626-33. doi: 10.1128/IAI.06061-11. Epub 2012 Feb 21.
3
In vitro-generated respiratory mucosa: a new tool to study inhalational anthrax.体外生成的呼吸道黏膜:一种研究吸入性炭疽的新工具。
Biochem Biophys Res Commun. 2003 Jun 6;305(3):624-32. doi: 10.1016/s0006-291x(03)00830-1.
4
Bacillus anthracis spore movement does not require a carrier cell and is not affected by lethal toxin in human lung models.炭疽芽孢杆菌孢子的移动不需要载体细胞,并且在人肺模型中不受致死毒素的影响。
Microbes Infect. 2016 Oct;18(10):615-626. doi: 10.1016/j.micinf.2016.06.004. Epub 2016 Jun 16.
5
Bacillus anthracis spore entry into epithelial cells is an actin-dependent process requiring c-Src and PI3K.炭疽芽孢杆菌孢子进入上皮细胞是一个依赖于肌动蛋白的过程,需要 c-Src 和 PI3K。
PLoS One. 2010 Jul 20;5(7):e11665. doi: 10.1371/journal.pone.0011665.
6
In vivo demonstration and quantification of intracellular Bacillus anthracis in lung epithelial cells.肺上皮细胞内炭疽芽孢杆菌的体内示踪与定量分析
Infect Immun. 2008 Sep;76(9):3975-83. doi: 10.1128/IAI.00282-08. Epub 2008 Jul 14.
7
Key aspects of the molecular and cellular basis of inhalational anthrax.吸入性炭疽病的分子和细胞基础的关键方面。
Microbes Infect. 2011 Dec;13(14-15):1146-55. doi: 10.1016/j.micinf.2011.07.005. Epub 2011 Jul 21.
8
Bacillus anthracis spores germinate extracellularly at air-liquid interface in an in vitro lung model under serum-free conditions.在无血清条件下的体外肺模型中,炭疽芽孢杆菌孢子在气液界面处进行胞外萌发。
J Appl Microbiol. 2015 Sep;119(3):711-23. doi: 10.1111/jam.12872. Epub 2015 Jul 30.
9
An integrated experimental-computational approach for predicting virulence in New Zealand white rabbits and humans following inhalation exposure to Bacillus anthracis spores.一种综合实验计算方法,用于预测新西兰白兔和人类在吸入炭疽芽孢杆菌孢子后感染的毒力。
PLoS One. 2019 Jul 1;14(7):e0219160. doi: 10.1371/journal.pone.0219160. eCollection 2019.
10
Bacillus anthracis has two independent bottlenecks that are dependent on the portal of entry in an intranasal model of inhalational infection.炭疽芽孢杆菌在经鼻吸入感染的模型中有两个独立的瓶颈,其取决于进入的门户。
Infect Immun. 2013 Dec;81(12):4408-20. doi: 10.1128/IAI.00484-13. Epub 2013 Sep 16.

引用本文的文献

1
Convergent evolution of diverse Bacillus anthracis outbreak strains toward altered surface oligosaccharides that modulate anthrax pathogenesis.不同炭疽杆菌暴发菌株向改变表面寡糖的趋同进化,这些寡糖调节炭疽病的发病机制。
PLoS Biol. 2020 Dec 28;18(12):e3001052. doi: 10.1371/journal.pbio.3001052. eCollection 2020 Dec.
2
Crossing of the epithelial barriers by Bacillus anthracis: the Known and the Unknown.炭疽芽孢杆菌跨越上皮屏障:已知与未知
Front Microbiol. 2015 Oct 9;6:1122. doi: 10.3389/fmicb.2015.01122. eCollection 2015.
3
Bacillus anthracis spores germinate extracellularly at air-liquid interface in an in vitro lung model under serum-free conditions.在无血清条件下的体外肺模型中,炭疽芽孢杆菌孢子在气液界面处进行胞外萌发。
J Appl Microbiol. 2015 Sep;119(3):711-23. doi: 10.1111/jam.12872. Epub 2015 Jul 30.
4
Deterministic models of inhalational anthrax in New Zealand white rabbits.新西兰白兔吸入性炭疽的确定性模型
Biosecur Bioterror. 2014 Jan-Feb;12(1):29-41. doi: 10.1089/bsp.2013.0067. Epub 2014 Feb 14.

本文引用的文献

1
In vivo demonstration and quantification of intracellular Bacillus anthracis in lung epithelial cells.肺上皮细胞内炭疽芽孢杆菌的体内示踪与定量分析
Infect Immun. 2008 Sep;76(9):3975-83. doi: 10.1128/IAI.00282-08. Epub 2008 Jul 14.
2
Microenvironmental impact on lung cell homeostasis and immunity during infection.感染期间微环境对肺细胞稳态和免疫的影响。
Expert Rev Vaccines. 2008 May;7(4):457-66. doi: 10.1586/14760584.7.4.457.
3
Potential dissemination of Bacillus anthracis utilizing human lung epithelial cells.利用人肺上皮细胞进行炭疽芽孢杆菌的潜在传播。
Cell Microbiol. 2008 Apr;10(4):945-57. doi: 10.1111/j.1462-5822.2007.01098.x. Epub 2007 Dec 6.
4
Lung dendritic cells rapidly mediate anthrax spore entry through the pulmonary route.肺树突状细胞通过肺部途径迅速介导炭疽芽孢进入。
J Immunol. 2007 Jun 15;178(12):7994-8001. doi: 10.4049/jimmunol.178.12.7994.
5
Human lung innate immune response to Bacillus anthracis spore infection.人类肺部对炭疽芽孢杆菌孢子感染的固有免疫反应。
Infect Immun. 2007 Aug;75(8):3729-38. doi: 10.1128/IAI.00046-07. Epub 2007 May 21.
6
Inactivation of Bacillus anthracis spores in murine primary macrophages.炭疽芽孢杆菌孢子在小鼠原代巨噬细胞中的失活
Cell Microbiol. 2006 Oct;8(10):1634-42. doi: 10.1111/j.1462-5822.2006.00738.x.
7
Roles of macrophages and neutrophils in the early host response to Bacillus anthracis spores in a mouse model of infection.巨噬细胞和中性粒细胞在小鼠感染炭疽芽孢杆菌孢子早期宿主反应中的作用。
Infect Immun. 2006 Jan;74(1):469-80. doi: 10.1128/IAI.74.1.469-480.2006.
8
Murine macrophages kill the vegetative form of Bacillus anthracis.小鼠巨噬细胞可杀死炭疽芽孢杆菌的繁殖体。
Infect Immun. 2005 Nov;73(11):7495-501. doi: 10.1128/IAI.73.11.7495-7501.2005.
9
The use of a model of in vivo macrophage depletion to study the role of macrophages during infection with Bacillus anthracis spores.使用体内巨噬细胞耗竭模型来研究巨噬细胞在炭疽芽孢杆菌孢子感染过程中的作用。
Microb Pathog. 2004 Oct;37(4):169-75. doi: 10.1016/j.micpath.2004.06.013.
10
In-vitro characterisation of the phagocytosis and fate of anthrax spores in macrophages and the effects of anti-PA antibody.巨噬细胞中炭疽芽孢吞噬作用及命运的体外特征分析以及抗保护性抗原(PA)抗体的影响
J Med Microbiol. 2002 Oct;51(10):821-831. doi: 10.1099/0022-1317-51-10-821.