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Infection and Immunity, February 2009, p. 604-614, Vol. 77, No. 2
0019-9567/09/$08.00+0     doi:10.1128/IAI.00907-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Interleukin-1 Receptor Signaling Protects Mice from Lethal Intestinal Damage Caused by the Attaching and Effacing Pathogen Citrobacter rodentium{triangledown}

Sarah L. Lebeis,1 Kimberly R. Powell,3 Didier Merlin,2 Melanie A. Sherman,3 and Daniel Kalman3*

Microbiology and Molecular Genetics Graduate Program, Emory University School of Medicine, 615 Michael Street, Whitehead Research Building No. 144, Atlanta, Georgia 30322,1 Department of Medicine, Emory University School of Medicine, 615 Michael Street, Whitehead Research Building, Atlanta, Georgia 30322,2 Department of Pathology and Laboratory Medicine, Emory University School of Medicine, 615 Michael Street, Whitehead Research Building No. 144, Atlanta, Georgia 303223

Received 22 July 2008/ Returned for modification 26 August 2008/ Accepted 21 November 2008

Enteropathogenic Escherichia coli, enterohemorrhagic E. coli, and Citrobacter rodentium are classified as attaching and effacing pathogens based on their ability to adhere to the intestinal epithelium via actin-filled membranous protrusions (pedestals). Infection of mice with C. rodentium causes a breach of the intestinal epithelial barrier, leading to colitis via a vigorous inflammatory response resulting in diarrhea and a protective antibody response that clears the pathogen. Here we show that interleukin-1 receptor (IL-1R) signaling protects mice following infection with C. rodentium. Upon infection, mice lacking the type I IL-1R exhibit increased mortality together with severe colitis characterized by intramural colonic bleeding and intestinal damage including gangrenous mucosal necrosis, phenotypes also evident in MyD88-deficient mice. However, unlike MyD88–/– mice, IL-1R–/– mice do not exhibit increased pathogen loads in the colon, delays in the recruitment of innate immune cells such as neutrophils, or defects in the capacity to replace damaged enterocytes. Further, we demonstrate that IL-1R–/– mice have an increased predisposition to intestinal damage caused by C. rodentium but not to that caused by chemical irritants, such as dextran sodium sulfate. Together, these data suggest that IL-1R signaling regulates the susceptibility of the intestinal epithelia to damage caused by C. rodentium.

* Corresponding author. Mailing address: Department of Pathology and Laboratory Medicine, Emory University School of Medicine, 615 Michael Street, Whitehead Research Building No. 144, Atlanta, GA 30322. Phone: (404) 712-2326. Fax: (404) 712-2979. E-mail: dkalman{at}emory.edu

{triangledown} Published ahead of print on 15 December 2008.

Editor: B. A. McCormick

Infection and Immunity, February 2009, p. 604-614, Vol. 77, No. 2
0019-9567/09/$08.00+0     doi:10.1128/IAI.00907-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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