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Infection and Immunity, June 2005, p. 3219-3227, Vol. 73, No. 6
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.6.3219-3227.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Salmonella enterica Serovar Typhimurium Pathogenicity Island 2 Is Necessary for Complete Virulence in a Mouse Model of Infectious Enterocolitis

Bryan Coburn,1 Yuling Li,1 David Owen,2 Bruce A. Vallance,3 and B. Brett Finlay1,4*

Michael Smith Laboratories and Department of Microbiology and Immunology,1 Department of Biochemistry and Molecular Biology, University of British Columbia, Vancouver, Canada,4 Department of Anatomical Pathology, Vancouver General Hospital, Vancouver, Canada,2 BC Research Institute, BC Children's and Women's Hospital, Vancouver, Canada3

Received 9 December 2004/ Returned for modification 21 January 2005/ Accepted 8 February 2005

Salmonella species cause a wide range of disease in multiple hosts. Salmonella enterica serovar Typhimurium causes self-limited intestinal disease in humans and systemic typhoid-like illness in susceptible mice. The prevailing dogma in murine S. enterica serovar Typhimurium pathogenesis is that distinct virulence mechanisms—Salmonella pathogenicity islands 1 and 2 (SPI1 and SPI2)—perform distinct roles in pathogenesis, the former being important for invasion and intestinal disease and the latter important for intracellular survival and systemic persistence and disease. Although evidence from bovine infections has suggested that SPI2 has a role in ileal disease, there is no evidence that SPI2 is important for inflammation in a disease that more closely recapitulates human colitis. Using S. enterica serovar Typhimurium strains that lack functional type III secretion systems, we demonstrate that SPI2 is essential for complete virulence in murine infectious enterocolitis. Using a recently characterized murine model (M. Barthel,S. Hapfelmeier, L. Quintanilla-Martinez, M. Kremer, M. Rohde, M. Hogardt, K. Pfeffer, H. Russmann, and W. D. Hardt, Infect. Immun. 71:2839-2858, 2003), we demonstrate that SPI1 mutants are unable to cause intestinal disease 48 h after infection and that SPI2-deficient bacteria also cause significantly attenuated typhlitis. We show that at the peak of inflammation in the cecum, SPI2 mutants induce diminished intercellular adhesion molecule 1 expression and neutrophil recruitment but that wild-type and mutant Salmonella are similarly distributed in the lumen of the infected organ. Finally, we demonstrate that attenuation of intestinal inflammation is accompanied by resolution of typhlitis in the mutant, but not wild-type, infections. Collectively, these results indicate that SPI2 is needed for enterocolitis, as well as for systemic disease.

* Corresponding author. Mailing address: Michael Smith Laboratories, University of British Columbia, 2185 East Mall, Vancouver, British Columbia V6T 1Z4, Canada. Phone: (604) 822-2493. Fax: (604) 822-9830. E-mail: bfinlay{at}interchange.ubc.ca.

Editor: D. L. Burns

Infection and Immunity, June 2005, p. 3219-3227, Vol. 73, No. 6
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.6.3219-3227.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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