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Infection and Immunity, May 2008, p. 2099-2105, Vol. 76, No. 5
0019-9567/08/$08.00+0     doi:10.1128/IAI.01137-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Genetic Resistance of Mice to Mycobacterium paratuberculosis Is Influenced by Slc11a1 at the Early but Not at the Late Stage of Infection{triangledown}

Virginie Roupie,1,{dagger} Valérie Rosseels,1,{dagger} Virginie Piersoel,1 Denise K. Zinniel,2 Raúl G. Barletta,2 and Kris Huygen1*

Mycobacterial Immunology, WIV-Pasteur Institute, 642 Engelandstraat, B1180 Brussels, Belgium,1 Department of Veterinary and Biomedical Sciences, University of Nebraska, Lincoln, Nebraska 68583-09052

Received 16 August 2007/ Returned for modification 10 October 2007/ Accepted 9 February 2008

We have recently described the development of a luminescent Mycobacterium paratuberculosis strain of bovine origin expressing the luxAB genes of Vibrio harveyi. With this luminescent isolate, fastidious and costly enumeration of CFU by plating them on agar can be replaced by easy and rapid luminometry. Here, we have reevaluated the effect of Slc11a1 (formerly Nramp1) polymorphism on susceptibility to M. paratuberculosis, using this luminometric method. A series of inbred mouse strains were infected intravenously with luminescent M. paratuberculosis S-23 and monitored for bacterial replication in spleen, liver, and lungs for 12 weeks. The results indicate that, as for Mycobacterium avium subsp. avium, innate resistance to infection is genetically controlled by Slc11a1. In BALB/c, congenic BALB.B10-H2b (BALB/c background; H-2b), C57BL/6, and beige C57BL/6bg/bg mice (all Slc11a1s), bacterial numbers in spleen and liver remained unchanged during the first 4 weeks of infection, whereas in DBA/2 and congenic BALB/c.DBA/2 (C.D2) mice (both Slc11a1r) and in (C57BL/6 x DBA/2)F1 mice (Slc11a1s/r), the bacterial numbers had decreased more than 10-fold at 4 weeks postinfection in both male and female mice. At later time points, additional differences in bacterial replication were observed between the susceptible mouse strains, particularly in the liver. Whereas bacterial numbers in the liver gradually decreased more than 100-fold in C57BL/6 mice between week 4 and week 12, bacterial numbers were stable in livers from BALB/c and beige C57BL/6bg/bg mice during this period. Mycobacterium-specific gamma interferon responses developed earlier and to a higher magnitude in C57BL/6 mice than in BALB/c mice and were lowest in resistant C.D2 mice.

* Corresponding author. Mailing address: Mycobacterial Immunology, WIV-Pasteur Institute, 642 Engelandstraat, B1180 Brussels, Belgium. Phone: 32 2 373 33 70. Fax: 32 2 373 33 67. E-mail: khuygen{at}pasteur.be

{triangledown} Published ahead of print on 19 February 2008.

Editor: J. L. Flynn

{dagger} V. Roupie and V. Rosseels contributed equally to this paper.

Infection and Immunity, May 2008, p. 2099-2105, Vol. 76, No. 5
0019-9567/08/$08.00+0     doi:10.1128/IAI.01137-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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