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Inhibition of expression of a staphylococcal superantigen-like protein by a soluble factor from Lactobacillus reuteri

Estelle Devillard^1,2,

¹ The Canadian Research and Development Centre for Probiotics, Lawson Health Research Institute, 268 Grosvenor St, London, Ontario, Canada N6A 4V2
² Department of Microbiology and Immunology, The University of Western Ontario, London, Ontario, Canada N6A 5C1
³ Infectious Diseases Research Group, The University of Western Ontario, London, Ontario, Canada N6A 5C1
⁴ Siebens-Drake Medical Research Institute, The University of Western Ontario, London, Ontario, Canada N6A 5C1
⁵ Department of Surgery, The University of Western Ontario, London, Ontario, Canada N6A 5C1

Correspondence
John K. McCormick
jmccormi{at}lri.sjhc.london.on.ca

Lactobacillus reuteri RC-14 has previously been shown to inhibit Staphylococcus aureus infection in a rat surgical-implant model. To investigate the basis for this, communication events between the two bacterial species were examined. L. reuteri RC-14 and Staph. aureus Newman were grown in a co-culture apparatus that physically separates the two species, while allowing the passage of soluble compounds. Using two-dimensional gel electrophoresis (2D-E), protein expression changes in Staph. aureus were analysed in response to co-culture with medium alone, L. reuteri RC-14, and a Lactobacillus strain that did not inhibit Staph. aureus infection in the rat model. It was observed that one protein in particular, identified as staphylococcal superantigen-like protein 11 (SSL11), showed a dramatic decrease in expression in response to growth with L. reuteri RC-14. Genetic reporters that placed both gfp and lux under the transcriptional control of the SSL11 promoter confirmed the 2D-E results. Interestingly, using similar reporter gene experiments, it was observed that the Staph. aureus P3 promoter from the staphylococcal accessory gene regulator (agr) locus also showed a decrease in expression in response to growth in the presence of L. reuteri RC-14. It was further demonstrated that L. reuteri RC-14 supernatant contained small unidentified molecules that were able to repress the SSL11 and P3 promoters, but the repression of SSL11 occurred independently of the agr system. These results suggest that L. reuteri RC-14 has the potential to alter the virulence of Staph. aureus via secretion of cell–cell signalling molecules.

Present address: The Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK.

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