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Infection and Immunity, March 2008, p. 907-915, Vol. 76, No. 3
0019-9567/08/$08.00+0     doi:10.1128/IAI.01432-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Enteric Salmonellosis Disrupts the Microbial Ecology of the Murine Gastrointestinal Tract

Department of Pediatrics, Division of Gastroenterology, The Medical College of Wisconsin, 8701 Watertown Plank Rd., Milwaukee, Wisconsin 53226,¹ Department of Cell Biology, Immunology Section, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands²

Received 24 October 2007/ Returned for modification 18 November 2007/ Accepted 10 December 2007

The commensal microbiota protects the murine host from enteric pathogens. Nevertheless, specific pathogens are able to colonize the intestinal tract and invade, despite the presence of an intact biota. Possibly, effective pathogens disrupt the indigenous microbiota, either directly through pathogen-commensal interaction, indirectly via the host mucosal immune response to the pathogen, or by a combination of these factors. This study investigates the effect of peroral Salmonella enterica serovar Typhimurium infection on the intestinal microbiota. Since the majority of the intestinal microbiota cannot be cultured by conventional techniques, molecular approaches using 16S rRNA sequences were applied. Several major bacterial groups were assayed using quantitative PCR. Administration of either the 50% lethal dose (LD₅₀) or 10x LD₅₀ of Salmonella enterica serovar Typhimurium caused changes in the microbiota throughout the intestinal tract over the time course of infection. A 95% decrease in total bacterial number was noted in the cecum and large intestine with 10x LD₅₀ S. enterica serovar Typhimurium challenge at 7 days postinfection, concurrent with gross evidence of diarrhea. In addition, alterations in microbiota composition preceded the onset of diarrhea, suggesting the involvement of pathogen-commensal interactions and/or host responses unrelated to diarrhea. Microbiota alterations were not permanent and reverted to the microbiota of uninfected mice by 1 month postinfection. Infection with a Salmonella pathogenicity island 1 (SPI1) mutant did not result in microbiota alterations, while SPI2 mutant infections triggered partial changes. Neither mutant was capable of prolonged colonization or induction of mucosal inflammation. These data suggest that several Salmonella virulence factors, particularly those involved in the local mucosal host response, are required for disruption of the intestinal ecosystem.

Published ahead of print on 26 December 2007.

Editor: A. J. Bäumler

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