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Infection and Immunity, May 2006, p. 2787-2802, Vol. 74, No. 5
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.5.2787-2802.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Influence of Slc11a1 on the Outcome of Salmonella enterica Serovar Enteritidis Infection in Mice Is Associated with Th Polarization

Judith Caron,1,2 Line Larivière,2 Mayss Nacache,1,2 Mifong Tam,2 Mary M. Stevenson,2,3,5 Colin McKerly,6 Philippe Gros,2,4 and Danielle Malo1,2,3*

Department of Human Genetics, McGill University, Montreal, Québec,1 Centre for the Study of Host Resistance, Montreal General Hospital, Montreal, Québec,2 Department of Medicine, McGill University, Montreal, Québec,3 Department of Biochemistry, McGill University, Montreal, Québec,4 Centre for Host-Parasite Interactions, McGill University, Macdonald Campus, Ste. Anne de Bellevue, Québec,6 Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada5

Received 21 November 2005/ Returned for modification 3 January 2006/ Accepted 22 February 2006

Genetic analyses identified Ses1 as a significant quantitative trait locus influencing the carrier state of 129S6 mice following a sublethal challenge with Salmonella enterica serovar Enteritidis. Previous studies have determined that Slc11a1 was an excellent candidate gene for Ses1. Kinetics of infection in 129S6 mice and Slc11a1-deficient (129S6-Slc11a1tm1Mcg) mice demonstrated that the wild-type allele of Slc11a1 contributed to the S. enterica serovar Enteritidis carrier state as early as 7 days postinfection. Gene expression profiling demonstrated that 129S6 mice had a significant up-regulation of proinflammatory genes associated with macrophage activation at day 10 postinfection, followed by a gradual increase in immunoglobulin transcripts, whereas 129S6-Slc11a1tm1Mcg mice had higher levels of immunoglobulins earlier in the infection. Quantitative reverse transcription-PCR revealed an increase in Th1 cytokine (Ifng and Il12) and Th1-specific transcription factor Tbx21 expression during infection in both the 129S6 and 129S6-Slc11a1tm1Mcg strains. However, the expression of Gata3, a transcription factor involved in Th2 polarization, Cd28, and Il4 was markedly increased in Slc11a1-deficient mice during infection, suggesting a predominant Th2 phenotype in 129S6-Slc11a1tm1Mcg animals following S. enterica serovar Enteritidis infection. A strong immunoglobulin G2a response, reflecting Th1 activity, was observed only in 129S6 mice. All together, these results are consistent with an impact of Slc11a1 on Th cell differentiation during chronic S. enterica serovar Enteritidis infection. The presence of a Th2 bias in Slc11a1-deficient mice is associated with improved bacterial clearance.

* Corresponding author. Mailing address: Departments of Medicine and Human Genetics, McGill University, McGill University Health Center, Montreal General Hospital, 1650 Cedar Avenue, local L11-144, Montreal, QC, Canada H3G 1A4. Phone: (514) 934-1934, ext. 44503. Fax: (514) 933-7146. E-mail: Danielle.malo{at}mcgill.ca.

Editor: A. D. O'Brien

Infection and Immunity, May 2006, p. 2787-2802, Vol. 74, No. 5
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.5.2787-2802.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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