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实验性小鼠布鲁氏菌病期间巨噬细胞的激活:慢性感染的基础

Macrophage activation during experimental murine brucellosis: a basis for chronic infection.

作者信息

Cheers C, Pagram F

出版信息

Infect Immun. 1979 Feb;23(2):197-205. doi: 10.1128/iai.23.2.197-205.1979.

Abstract

Evidence is presented that the chronicity of infection in CBA mice after injection of Brucella abortus 19 is related to a number of factors: (i) the relative resistance of B. abortus to macrophage killing, which allowed some bacteria to survive the peak of macrophage activity occurring at 14 days; (ii) the decline in macrophage activity thereafter (this decline was related in part to the presence of fewer bacteria to stimulate the bactericidal activity and also to specific, active suppressor mechanisms not identified in this study); and (iii) the insensitivity of the persistent Brucella organisms to activated macrophages. This was not due to a selection of genetically resistant bacteria, but possibly to their inaccessibility, either within "incompetent" macrophages or outside macrophages altogether.

摘要

有证据表明,注射流产布鲁氏菌19株后,CBA小鼠感染的慢性化与多种因素有关:(i)流产布鲁氏菌对巨噬细胞杀伤的相对抗性,这使得一些细菌能够在14天时巨噬细胞活性高峰时存活下来;(ii)此后巨噬细胞活性下降(这种下降部分与刺激杀菌活性的细菌数量减少有关,也与本研究中未确定的特定活性抑制机制有关);(iii)持续存在的布鲁氏菌对活化巨噬细胞不敏感。这并非由于选择了具有遗传抗性的细菌,而是可能由于它们难以接近,要么在“无功能的”巨噬细胞内,要么完全在巨噬细胞外。

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