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Infection and Immunity, April 2007, p. 1994-2003, Vol. 75, No. 4
0019-9567/07/$08.00+0     doi:10.1128/IAI.01216-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

A MyD88-Deficient Mouse Model Reveals a Role for Nramp1 in Campylobacter jejuni Infection{triangledown}

Robert O. Watson, Veronica Novik, Dirk Hofreuter, María Lara-Tejero, and Jorge E. Galán*

Section of Microbial Pathogenesis, Yale University, School of Medicine, New Haven, Connecticut 06536

Received 1 August 2006/ Returned for modification 17 September 2006/ Accepted 14 December 2006

Campylobacter jejuni is a major worldwide cause of enteric illnesses. Adult immunocompetent mice are not susceptible to C. jejuni infection. However, we show here that mice deficient in the adaptor protein myeloid differentiation factor 88 (MyD88), which is required for signaling through most Toll-like receptors, can be stably colonized by C. jejuni but not by isogenic derivatives carrying mutations in known virulence genes. We also found that Nramp1 deficiency increases the mouse susceptibility to C. jejuni infection when administered systemically. These results indicate that MyD88-deficient mice could be a useful model to study C. jejuni colonization and reveal a potential role for Nramp1 in the control of this bacterial pathogen.

* Corresponding author. Mailing address: Section of Microbial Pathogenesis, Yale University, School of Medicine, New Haven, CT 06536. Phone: (203) 737-2404. Fax: (203) 737-2630. E-mail: jorge.galan{at}yale.edu.

{triangledown} Published ahead of print on 28 December 2007.

Editor: A. Camilli

Infection and Immunity, April 2007, p. 1994-2003, Vol. 75, No. 4
0019-9567/07/$08.00+0     doi:10.1128/IAI.01216-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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