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Infect. Immun. doi:10.1128/IAI.01432-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. 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, WI 53226; Department of Cell Biology, Immunology Section, University Medical Center Groningen, University of Groningen, the Netherlands

^* To whom correspondence should be addressed. Email: nsalzman{at}mcw.edu.

	Abstract

Commensal microbiota protect the murine host from enteric pathogens. Nevertheless, specfic 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 host mucosal immune response to the pathogen, or by a combination of these factors. This study investigates the effect of per oral 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 LD₅₀ or 10XLD₅₀ dose of Salmonella typhimurium caused changes in the microbiota throughout the intestinal tract over the time course of infection. A 95% decrease in total bacterial numbers was noted in the cecum and large intestine with 10XLD₅₀ S. typhimurium challenge 7 days post infection, concurrent with gross evidence of diarrhea. In addition, alterations in microbiota composition precede 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 that of uninfected mice one month post infection. Infection with a SPI1 mutant did not result in microbiota alterations, while SPI2 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 local mucosal host response, are required for disruption of the intestinal ecosystem.

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