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Appl Environ Microbiol, April 1998, p. 1323-1327, Vol. 64, No. 4
0099-2240/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

A Competitive Microflora Increases the Resistance of Salmonella typhimurium to Inimical Processes: Evidence for a Suicide Response

Timothy G. Aldsworth, Rachel L. Sharman, Christine E. R. Dodd, and Gordon S. A. B. Stewart*

Department of Applied Biochemistry and Food Science, University of Nottingham, Sutton Bonington Campus, Loughborough, Leicestershire, LE12 5RD, United Kingdom

Received 12 November 1997/Accepted 3 February 1998

The presence of a viable competitive microflora at cell densities of 108 CFU ml-1 protects an underlying population of 105 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°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.


* Corresponding author. Mailing address: Dept. of Applied Biochemistry and Food Science, University of Nottingham, Sutton Bonington Campus, Loughborough, Leicestershire, LE12 5RD, United Kingdom. Phone: (0115) 951 6165. Fax: (0115) 951 6162. E-mail: Gordon.Stewart{at}NOTTINGHAM.AC.UK.




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