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炭疽水肿毒素使DBA/2J小鼠对致死毒素敏感。

Anthrax edema toxin sensitizes DBA/2J mice to lethal toxin.

作者信息

Firoved Aaron M, Moayeri Mahtab, Wiggins Jason F, Shen Yuequan, Tang Wei-Jen, Leppla Stephen H

机构信息

National Institute of Allergy and Infectious Diseases, National Institutes of Health, 30 Convent Dr., Building 30, Room 303, Bethesda, MD 20892-4349, USA.

出版信息

Infect Immun. 2007 May;75(5):2120-5. doi: 10.1128/IAI.01781-06. Epub 2007 Mar 5.

Abstract

Anthrax toxin is made up of three separate protein components: the receptor-binding protective antigen (PA), the adenylyl cyclase edema factor (EF), and the metalloproteinase lethal factor (LF). EF and PA constitute edema toxin (ET), which causes edema when injected subcutaneously. At higher doses, ET causes severe pathologies and death in BALB/cJ mice (A. M. Firoved et al., Am. J. Pathol. 167:1309-1320, 2005). A striking effect of ET at lethal doses is adrenal necrosis. Here we show that low doses of ET (10 microg) that produce no overt signs of illness in mice still cause substantial adrenal lesions. These lesions are not associated with reduced corticosterone production; instead, ET-treated mice have increased corticosterone production. Because the resistance of mice to the other component of anthrax toxin, lethal toxin (LT; LF plus PA), has been shown to be overcome by the perturbation of the endocrine system, we hypothesized that sublethal doses of ET might sensitize LT-resistant DBA/2J mice to LT-mediated lethality. We report that a low dose of ET (5 microg) is sufficient to sensitize DBA/2J mice when given concurrently with LT. Higher doses of ET (e.g., 15 microg) given to male and female DBA/2J mice 18 h prior to LT challenge also sensitize them to LT. This study using highly purified ET and LT demonstrates how the components of anthrax toxin can work together to increase lethality.

摘要

炭疽毒素由三种不同的蛋白质成分组成

受体结合保护性抗原(PA)、腺苷酸环化酶水肿因子(EF)和金属蛋白酶致死因子(LF)。EF和PA构成水肿毒素(ET),皮下注射时会导致水肿。在较高剂量下,ET会在BALB/cJ小鼠中引起严重病变并导致死亡(A.M.菲罗韦德等人,《美国病理学杂志》167:1309 - 1320,2005年)。ET在致死剂量下的一个显著作用是肾上腺坏死。在此我们表明,低剂量的ET(10微克)在小鼠中不会产生明显的疾病迹象,但仍会导致大量肾上腺损伤。这些损伤与皮质酮分泌减少无关;相反,经ET处理的小鼠皮质酮分泌增加。由于已表明小鼠对炭疽毒素的另一种成分致死毒素(LT;LF加PA)的抗性可通过内分泌系统的扰动而被克服,我们推测亚致死剂量的ET可能会使对LT有抗性的DBA/2J小鼠对LT介导的致死性敏感。我们报告,当与LT同时给予时,低剂量的ET(5微克)足以使DBA/2J小鼠敏感。在LT攻击前18小时给雄性和雌性DBA/2J小鼠注射更高剂量的ET(例如15微克)也会使它们对LT敏感。这项使用高度纯化的ET和LT的研究证明了炭疽毒素的成分如何协同作用以增加致死性。

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