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Infection and Immunity, April 2003, p. 1849-1855, Vol. 71, No. 4
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.4.1849-1855.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Development and Evaluation of an Improved Mouse Model of Meningococcal Colonization

Kyungcheol Yi,1* David S. Stephens,1,2,3 and Igor Stojiljkovic1

Department of Microbiology and Immunology,1 Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia 30322,2 Laboratories of Microbial Pathogenesis, Veterans Affairs Medical Center, Atlanta, Georgia 303033

Received 30 October 2002/ Returned for modification 16 December 2002/ Accepted 14 January 2003

Studies of meningococcal pathogenesis have been severely restricted due to the absence of an adequate animal model. Given the significance of iron in meningococcal pathogenesis, we developed a model of Neisseria meningitidis colonization in outbred adult mice that included daily administration of iron dextran. While receiving iron, the animals were inoculated intranasally with the initial doses of bacterial suspension. Meningococci were recovered from the animals by nasopharyngeal washes. Approximately half of the animals inoculated with 107 CFU remained colonized 13 days after the initial bacterial inoculation. The model was further evaluated with genetically defined isogenic serogroup B mutant strains, and the colonization capabilities of the mutants were compared to that of the wild-type parent. A mutant that produces truncated lipooligosaccharide (KDO2-lipid A) and a mutant defective in capsule transport were dramatically impaired in colonization. A mutant defective in pilus transport (pilQ) showed moderately impaired colonization. The immunological aspect of the model was also evaluated by challenging mice after immunization with homologous whole-cell meningococci. The immunized mice were protected from colonization of the homologous strain. In this model, long-term meningococcal colonization was maintained, allowing us to study the effects of specific genetic mutation on colonization. In addition, this model allows investigation of the role of active immune response against meningococci.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Emory University School of Medicine, 1510 Clifton Rd. NE, Atlanta, GA 30322. Phone: (404) 727-5968. Fax: (404) 727-3659. E-mail: kyi{at}emory.edu.

Editor: F. C. Fang

Infection and Immunity, April 2003, p. 1849-1855, Vol. 71, No. 4
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.4.1849-1855.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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