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Applied and Environmental Microbiology, May 2003, p. 2692-2698, Vol. 69, No. 5
0099-2240/03/$08.00+0     DOI: 10.1128/AEM.69.5.2692-2698.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Role of Listeria monocytogenes {sigma}B in Survival of Lethal Acidic Conditions and in the Acquired Acid Tolerance Response

Adriana Ferreira,1 David Sue,1 Conor P. O'Byrne,2 and Kathryn J. Boor1*

Department of Food Science, Cornell University, Ithaca, New York 14853,1 Department of Microbiology, National University of Ireland, Galway, Ireland2

Received 27 August 2002/ Accepted 3 February 2003

The food-borne pathogen Listeria monocytogenes can acquire enhanced resistance to lethal acid conditions through multiple mechanisms. We investigated contributions of the stress-responsive alternative sigma factor, {sigma}B, which is encoded by sigB, to growth phase-dependent acid resistance (AR) and to the adaptive acid tolerance response in L. monocytogenes. At various points throughout growth, we compared the relative survival of L. monocytogenes wild-type and {Delta}sigB strains that had been exposed to either brain heart infusion (pH 2.5) or synthetic gastric fluid (pH 2.5) with and without prior acid adaptation. Under these conditions, survival of the {Delta}sigB strain was consistently lower than that of the wild-type strain throughout all phases of growth, ranging from 4 orders of magnitude less in mid-log phase to 2 orders of magnitude less in stationary phase. Survival of both {Delta}sigB and wild-type L. monocytogenes strains increased by 6 orders of magnitude upon entry into stationary phase, demonstrating that the L. monocytogenes growth phase-dependent AR mechanism is {sigma}B independent. {sigma}B-mediated contributions to acquired acid tolerance appear to be greatest in early logarithmic growth. Loss of a functional {sigma}B reduced the survival of L. monocytogenes at pH 2.5 to a greater extent in the presence of organic acid (100 mM acetic acid) than in the presence of inorganic acid alone (HCl), suggesting that L. monocytogenes protection against organic and inorganic acid may be mediated through different mechanisms. {sigma}B does not appear to contribute to pHi homeostasis through regulation of net proton movement across the cell membrane or by regulation of pHi buffering by the GAD system under the conditions examined in this study. In summary, a functional {sigma}B protein is necessary for full resistance of L. monocytogenes to lethal acid treatments.

* Corresponding author. Mailing address: Department of Food Science, 413 Stocking Hall, Cornell University, Ithaca, NY 14853. Phone: (607) 255-3111. Fax: (607) 254-4868. E-mail: kjb4{at}cornell.edu.

Applied and Environmental Microbiology, May 2003, p. 2692-2698, Vol. 69, No. 5
0099-2240/03/$08.00+0     DOI: 10.1128/AEM.69.5.2692-2698.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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