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Infection and Immunity, July 2009, p. 2932-2942, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.00172-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

The Capsule-Encoding viaB Locus Reduces Intestinal Inflammation by a Salmonella Pathogenicity Island 1-Independent Mechanism{triangledown}

Takeshi Haneda, Sebastian E. Winter, Brian P. Butler, R. Paul Wilson, Çagla Tükel, Maria G. Winter, Ivan Godinez, Renée M. Tsolis, and Andreas J. Bäumler*

Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Ave., Davis, California

Received 13 February 2009/ Returned for modification 19 March 2009/ Accepted 3 May 2009

Salmonella enterica serotype Typhimurium elicits acute neutrophil influx in the human intestinal mucosa within 1 or 2 days after infection, resulting in inflammatory diarrhea. In contrast, no overt symptoms are observed within the first 1 or 2 weeks after infection with S. enterica serotype Typhi. Here we show that introduction of the capsule-encoding viaB locus of serotype Typhi reduced the ability of serotype Typhimurium to elicit acute intestinal inflammation in a streptomycin-pretreated mouse model. Serotype Typhimurium requires a functional invasion-associated type III secretion system (type III secretion system 1 [T3SS-1]) to elicit cecal inflammation within 48 h after infection of streptomycin-pretreated mice, and the presence of the viaB locus reduced its invasiveness for human intestinal epithelial cells in vitro. However, a reduced activity of T3SS-1 could not account for the ability of the viaB locus to attenuate cecal inflammation, because introduction of the viaB locus into an invasion-deficient serotype Typhimurium strain (invA mutant) resulted in a significant reduction of pathology and inflammatory cytokine expression in the cecum 5 days after infection of mice. We conclude that a T3SS-1-independent mechanism contributes to the ability of the viaB locus to reduce intestinal inflammation.

* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Ave., Davis, CA 95616-8645. Phone: (530) 754-7225. Fax: (530) 754-7240. E-mail: ajbaumler{at}ucdavis.edu

{triangledown} Published ahead of print on 18 May 2009.

Editor: J. B. Bliska

Infection and Immunity, July 2009, p. 2932-2942, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.00172-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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