Dodd Christine E R, Richards Philip J, Aldsworth Timothy G
Division of Food Sciences, School of Biosciences, University of Nottingham, Sutton Bonington Campus, Loughborough, Leicestershire LE12 5RD, UK.
Int J Food Microbiol. 2007 Nov 30;120(1-2):46-50. doi: 10.1016/j.ijfoodmicro.2007.06.008. Epub 2007 Jun 13.
The response of bacteria to sub-lethal injury is an important aspect of food microbiology as many inimical processes to which bacteria are subjected during processing are non-lethal. For pathogens like Salmonella and Escherichia coli, the difference in injury levels of exponential phase cells compared to their stationary phase counterparts in this regard is well recognised and evident for a variety of inimical processes. The expression of a range of stress resistance genes under the control of the sigma factor RpoS provides some explanation for the greater resistance of stationary phase cells. However in 1997 the suicide response hypothesis was put forward as an explanation for the observed response of Salmonella and E. coli to sub-lethal stresses. This hypothesis arose as an explanation for the observed protection of Salmonella and E. coli strains to heat and freeze-thaw injury by the presence of a high level of competitor organisms, a protection that had been shown to be RpoS independent. The central tenet of this theory was that under sub-lethal stress bacteria produce a burst of intracellular free radicals and it is these that lead to sub-lethal injury and/or death. Exponential phase cells because of their more active metabolism are more susceptible to this effect and suffer greater damage. This paper reviews the origins of this theory, the evidence for a free radical response and explores the potential mechanisms by which competitor cells produce a protective effect.
细菌对亚致死损伤的反应是食品微生物学的一个重要方面,因为在加工过程中细菌所经历的许多有害过程都是非致死性的。对于沙门氏菌和大肠杆菌等病原体而言,在这方面指数生长期细胞与稳定期细胞损伤水平的差异已得到充分认识,并且在各种有害过程中都很明显。在σ因子RpoS控制下一系列抗逆基因的表达,为稳定期细胞具有更强抗性提供了一些解释。然而在1997年,自杀反应假说被提出,以解释观察到的沙门氏菌和大肠杆菌对亚致死应激的反应。这个假说的提出是为了解释观察到的高水平竞争生物体的存在对沙门氏菌和大肠杆菌菌株起到的热保护及冻融损伤保护作用,这种保护已被证明与RpoS无关。该理论的核心观点是,在亚致死应激下,细菌会产生一阵细胞内自由基,正是这些自由基导致亚致死损伤和/或死亡。指数生长期细胞由于其代谢更活跃,更容易受到这种影响,遭受的损伤也更大。本文回顾了该理论的起源、自由基反应的证据,并探讨了竞争细胞产生保护作用的潜在机制。