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Journal of Bacteriology, June 2008, p. 4233-4241, Vol. 190, No. 12
0021-9193/08/$08.00+0     doi:10.1128/JB.00205-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Formate Acts as a Diffusible Signal To Induce Salmonella Invasion{triangledown}

Yanyan Huang,1,2 Mitsu Suyemoto,2 Cherilyn D. Garner,1 Kellie M. Cicconi,1 and Craig Altier1*

Department of Population Medicine and Diagnostic Sciences, Cornell University, Ithaca, New York 14853,1 College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 276062

Received 9 February 2008/ Accepted 9 April 2008

To infect an animal host, Salmonella enterica serovar Typhimurium must penetrate the intestinal epithelial barrier. This process of invasion requires a type III secretion system encoded within Salmonella pathogenicity island I (SPI1). We found that a mutant with deletions of the acetate kinase and phosphotransacetylase genes (ackA-pta) was deficient in invasion and SPI1 expression but that invasion gene expression was completely restored by supplying medium conditioned by growth of the wild-type strain, suggesting that a signal produced by the wild type, but not by the ackA-pta mutant, was required for invasion. This mutant also excreted 68-fold-less formate into the culture medium, and the addition of sodium formate to cultures restored both the expression of SPI1 and the invasion of cultured epithelial cells by the mutant. The effect of formate was pH dependent, requiring a pH below neutrality, and studies in mice showed that the distal ileum, the preferred site of Salmonella invasion in this species, had the appropriate formate concentration and pH to elicit invasion, while the cecum contained no detectable formate. Furthermore, we found that formate affected the major regulators of SPI1, hilA and hilD, but that the primary routes of formate metabolism played no role in its activity as a signal.

* Corresponding author. Mailing address: Department of Population Medicine and Diagnostic Sciences, Upper Tower Road, Cornell University, Ithaca, NY 14853. Phone: (607) 253-3926. Fax: (607) 253-3907. E-mail: ca223{at}cornell.edu

{triangledown} Published ahead of print on 18 April 2008.

Journal of Bacteriology, June 2008, p. 4233-4241, Vol. 190, No. 12
0021-9193/08/$08.00+0     doi:10.1128/JB.00205-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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