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Infection and Immunity, December 2007, p. 5609-5614, Vol. 75, No. 12
0019-9567/07/$08.00+0     doi:10.1128/IAI.00781-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Transgenic Mice Expressing Human Transferrin as a Model for Meningococcal Infection{triangledown}

Maria-Leticia Zarantonelli,1 Marek Szatanik,1 Dario Giorgini,1 Eva Hong,1 Michel Huerre,2 Florian Guillou,3 Jean-Michel Alonso,1 and Muhamed-Kheir Taha1*

Neisseria Unit, National Reference Centre for the Meningococci,1 Histopathology Unit, Institut Pasteur, 25-28 rue du Dr. Roux, 75724 Paris cedex 15, France,2 UMR 6175, Institut National de la Recherche Agronomique, Centre National de Recherche Scientifique, Université de Tours, Haras Nationaux, Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France3

Received 8 June 2007/ Returned for modification 4 July 2007/ Accepted 13 September 2007

The pathogenesis of meningococcal disease is poorly understood due to the lack of a relevant animal model. Moreover, the use of animal models is not optimal as most meningococcal virulence determinants recognize receptors that are specifically expressed in human tissues. One major element of the host specificity is the system of meningococcal iron uptake by transferrin-binding proteins that bind specifically human transferrin but not murine transferrin. We developed a new mouse model for experimental meningococcal infection using transgenic mice expressing human transferrin. Intraperitoneal challenge of transgenic mice induced bacteremia for at least 48 h with an early stage of multiplication, whereas the initial inoculum was rapidly cleared from blood in wild-type mice. Inflammation in the subarachnoidal space with a high influx of polymorphonuclear cells was observed only in transgenic mice. Meningococcal mutants that were unable to use transferrin as a source of iron were rapidly cleared from both wild-type and transgenic mice. Thus, transgenic mice expressing human transferrin may represent an important advance as a new mouse model for in vivo studies of meningococcal virulence and immunogenicity factors.

* Corresponding author. Mailing address: Neisseria Unit, National Reference Centre for the Meningococci, Institut Pasteur, 25-28 rue du Dr. Roux, 75724 Paris cedex 15, France. Phone: 33 1 44 38 95 90. Fax: 33 1 45 68 83 38. E-mail: mktaha{at}pasteur.fr

{triangledown} Published ahead of print on 24 September 2007.

Editor: R. P. Morrison

Infection and Immunity, December 2007, p. 5609-5614, Vol. 75, No. 12
0019-9567/07/$08.00+0     doi:10.1128/IAI.00781-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Granoff, D. M., Welsch, J. A., Ram, S. (2009). Binding of Complement Factor H (fH) to Neisseria meningitidis Is Specific for Human fH and Inhibits Complement Activation by Rat and Rabbit Sera. Infect. Immun. 77: 764-769 [Abstract] [Full Text]  


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