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竞争性微生物群落增强了鼠伤寒沙门氏菌对有害过程的抗性:自杀反应的证据。

A competitive microflora increases the resistance of Salmonella typhimurium to inimical processes: evidence for a suicide response.

作者信息

Aldsworth T G, Sharman R L, Dodd C E, Stewart G S

机构信息

Department of Applied Biochemistry and Food Science, University of Nottingham, Loughborough, Leicestershire, United Kingdom.

出版信息

Appl Environ Microbiol. 1998 Apr;64(4):1323-7. doi: 10.1128/AEM.64.4.1323-1327.1998.

Abstract

The presence of a viable competitive microflora at cell densities of 10(8) CFU ml-1 protects an underlying population of 10(5) CFU of Salmonella typhimurium ml-1 against freeze injury. The mechanism of enhanced resistance was initially postulated to be via an RpoS-mediated adaptive response. By using an spvRA:: luxCDABE reporter we have shown that although the onset of RpoS-mediated gene expression was brought forward by the addition of a competitive microflora, the time taken for induction was measured in hours. Since the protective effect of a competitive microflora is essentially instantaneous, the stationary-phase adaptive response is excluded as the physiological mechanism. The only instantaneous effect of the competitive microflora was a reduction in the percent saturation of oxygen from 100% to less than 10%. For both mild heat treatment (55 degrees C) and freeze injury this change in oxygen tension affords Salmonella a substantive (2 orders of magnitude) enhancement in survival. By reducing the levels of dissolved oxygen through active respiration, a competitive microflora reduces oxidative damage to exponential-phase cells irrespective of the inimical treatment. These results have led us to propose a suicide hypothesis for the destruction of rapidly growing cells by inimical processes. In essence, the suicide hypothesis proposes that a mild inimical process leads to the growth arrest of exponential-phase cells and to the decoupling of anabolic and catabolic metabolism. The result of this is a free radical burst which is lethal to unadapted cells.

摘要

细胞密度为10(8) CFU/ml的有活力的竞争性微生物群落的存在,可保护10(5) CFU/ml的鼠伤寒沙门氏菌下层菌群体免受冻害。增强抗性的机制最初被假定为通过RpoS介导的适应性反应。通过使用spvRA::luxCDABE报告基因,我们已经表明,尽管添加竞争性微生物群落提前了RpoS介导的基因表达的起始时间,但诱导所需的时间是以小时来衡量的。由于竞争性微生物群落的保护作用基本上是瞬时的,因此排除了稳定期适应性反应作为生理机制。竞争性微生物群落的唯一瞬时效应是氧气饱和度百分比从100%降至10%以下。对于温和热处理(55℃)和冻害,这种氧张力的变化都使沙门氏菌的存活率有实质性(2个数量级)的提高。通过主动呼吸降低溶解氧水平,竞争性微生物群落可减少对指数生长期细胞的氧化损伤,而与有害处理无关。这些结果使我们提出了一个自杀假说,用于解释有害过程对快速生长细胞的破坏。本质上,自杀假说提出,轻度有害过程会导致指数生长期细胞的生长停滞以及合成代谢和分解代谢的解偶联。其结果是自由基爆发,这对未适应的细胞是致命的。

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