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Infection and Immunity, June 2005, p. 3228-3241, Vol. 73, No. 6
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.6.3228-3241.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Comparison of Salmonella enterica Serovar Typhimurium Colitis in Germfree Mice and Mice Pretreated with Streptomycin

Bärbel Stecher,¹ Andrew J. Macpherson,^2, Siegfried Hapfelmeier,¹ Marcus Kremer,³ Thomas Stallmach,⁴ and Wolf-Dietrich Hardt^1*

Institute of Microbiology, D-BIOL, ETH Zürich, Wolfgang-Paulistrasse 10, CH-8093 Zürich, Switzerland,¹ Institute of Experimental Immunology, Universitätsspital Zürich, Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland,² Institute of Pathology, Technische Universität München, Ismaninger Strasse 22, D-81675 München, Germany,³ Institute of Clinical Pathology, Universitätsspital Zürich, Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland⁴

Received 31 August 2004/ Returned for modification 21 October 2004/ Accepted 2 February 2005

Salmonella enterica subspecies 1 serovar Typhimurium is a common cause of bacterial enterocolitis. Mice are generally protected from Salmonella serovar Typhimurium colonization and enterocolitis by their resident intestinal microflora. This phenomenon is called "colonization resistance" (CR). Two murine Salmonella serovar Typhimurium infection models are based on the neutralization of CR: (i) in specific-pathogen-free mice pretreated with streptomycin (StrSPF mice) antibiotics disrupt the intestinal microflora; and (ii) germfree (GF) mice are raised without any intestinal microflora, but their intestines show distinct physiologic and immunologic characteristics. It has been unclear whether the same pathogenetic mechanisms trigger Salmonella serovar Typhimurium colitis in GF and StrSPF mice. In this study, we compared the two colitis models. In both of the models Salmonella serovar Typhimurium efficiently colonized the large intestine and triggered cecum and colon inflammation starting 8 h postinfection. The type III secretion system encoded in Salmonella pathogenicity island 1 was essential in both disease models. Thus, Salmonella serovar Typhimurium colitis is triggered by similar pathogenetic mechanisms in StrSPF and GF mice. This is remarkable considering the distinct physiological properties of the GF mouse gut. One obvious difference was more pronounced damage and reduced regenerative response of the cecal epithelium in GF mice. Overall, StrSPF mice and GF mice provide similar but not identical models for Salmonella serovar Typhimurium colitis.

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* Corresponding author. Mailing address: Institute of Microbiology, ETH Zürich, Wolfgang-Paulistrasse 10, HCI G413, CH-8093 Zürich, Switzerland. Phone: 01-632-5143. Fax: 01-632-1129. E-mail: hardt{at}micro.biol.ethz.ch.

Editor: J. B. Bliska

Present address: McMaster University, 1200 Main St. W., HSC 3N51, Hamilton, ON, L8N 3Z5 Canada.

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Infection and Immunity, June 2005, p. 3228-3241, Vol. 73, No. 6
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.6.3228-3241.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

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