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Infection and Immunity, January 2009, p. 214-222, Vol. 77, No. 1
0019-9567/09/$08.00+0     doi:10.1128/IAI.01066-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Interleukin-15 and NK1.1+ Cells Provide Innate Protection against Acute Salmonella enterica Serovar Typhimurium Infection in the Gut and in Systemic Tissues{triangledown}

Ali A. Ashkar,1,{dagger}* Sarah Reid,1 Elena F. Verdu,2 Kun Zhang,3 and Brian K. Coombes3,{dagger}*

Department of Pathology and Molecular Medicine,1 Department of Medicine,2 the Michael DeGroote Institute for Infectious Disease Research, Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON L8N 3Z5, Canada3

Received 27 August 2008/ Returned for modification 2 October 2008/ Accepted 31 October 2008

Control of bacterial colonization at mucosal surfaces depends on rapid activation of the innate immune system. Interleukin-15 (IL-15) directs the development, maturation, and function of a population of cells positive for NK1.1, such as natural killer (NK) cells, which are critical components of the innate immune defense against several viral and bacterial pathogens. Using IL-15-deficient mice, in vivo depletion of NK1.1+ cells from wild-type mice, and in vivo overexpression of IL-15 from a recombinant adenovirus, we tested the role of IL-15 and NK1.1+ cells in innate protection of the murine gut and reticuloendothelial system from Salmonella enterica serovar Typhimurium infection. IL-15 and the NK1.1+ cell population provided innate protection from serovar Typhimurium in mice at the enteric mucosae and in the reticuloendothelial system during murine typhoid. Interestingly, serovar Typhimurium extensively colonized the gut of IL-15–/– mice and wild-type C57BL/6 mice depleted of NK1.1+ cells prior to infection, even though the animals were not pretreated with antibiotics to reduce colonization resistance and there was an absence of overt inflammation in the colon and cecum. Enhanced dissemination of Salmonella from the gut of mice depleted of NK1.1+ cells correlated with a localized disruption of IL-17 in the colon. These data suggest a relationship between the gut ecosystem and the innate mucosal immune system, which may be linked via IL-15 and NK1.1+ cells.

* Corresponding author. Mailing address for Brian K. Coombes: Biochemistry & Biomedical Sciences, McMaster University, HSC-4H17, 1200 Main St. West, Hamilton, Ontario L8N 3Z5, Canada. Phone: (905) 525-9140, ext. 22159. Fax: (905) 522-9033. E-mail: coombes{at}mcmaster.ca. Mailing address for Ali Ashkar: Pathology & Molecular Medicine, McMaster University MDCL-4015, 1200 Main St. West, Hamilton, ON L8N 3Z5, Canada. Phone: (905) 525-9140. Fax: (905) 522-6750. E-mail: ashkara{at}mcmaster.ca

{triangledown} Published ahead of print on 17 November 2008.

Editor: A. J. Bäumler

{dagger} Contributed equally.

Infection and Immunity, January 2009, p. 214-222, Vol. 77, No. 1
0019-9567/09/$08.00+0     doi:10.1128/IAI.01066-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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