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Infection and Immunity, September 2006, p. 5261-5271, Vol. 74, No. 9
0019-9567/06/$08.00+0     doi:10.1128/IAI.01094-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Campylobacter jejuni Colonization of Mice with Limited Enteric Flora

Christopher Chang1,2* and Jeff F. Miller1

Department of Microbiology, Immunology, and Molecular Genetics,1 Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California 900952

Received 12 July 2005/ Returned for modification 16 January 2006/ Accepted 21 June 2006

We have developed experimental murine Campylobacter infection models which demonstrate efficient establishment and reproducible, high-level colonization. Following oral inoculation, wild-type C3H mice with normal enteric flora were colonized inconsistently and inefficiently by C. jejuni strain 81-176. However, C3H mice with a limited gut flora (LF) were efficiently colonized at high levels (108 CFU/g of stool or large intestine tissue) followed by clearance after several weeks. Large intestine tissue showed minimal to mild inflammation at days 7 and 28 postinoculation. In striking contrast, C3H SCID mice with the same limited flora remained persistently colonized at a consistently high level until they were euthanized 8 months postinoculation. Lower gastrointestinal tract tissue from LF-SCID mice showed marked to severe inflammation in the colon and cecum at days 7 and 28 and intense inflammation of the stomach at day 28. These findings indicate that although the innate response alone cannot block colonization persistence, it is sufficient to orchestrate marked gut inflammation. Moreover, the adaptive immune response is critical to mediate C. jejuni clearance from the colonized gut. To validate our LF murine model, we verified that motility and chemotaxis are critical for colonization. Insertion-deletion mutations were generated in motB and fliI, which encode products essential for motility and flagellar assembly, and in the presumptive chemotaxis gene cheA (histidine kinase). All mutants failed to establish colonization in LF mice. Our limited flora murine colonization models serve as tractable, reproducible tools to define host responses to C. jejuni infection and to identify and characterize virulence determinants required for colonization.

* Corresponding author. Mailing address: Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine at UCLA, 10833 Le Conte Ave., CHS 43-326, Los Angeles, CA 90095-1747. Phone: (310) 206-9053. Fax: (310) 267-2774. E-mail: gichang{at}ucla.edu.

Editor: V. J. DiRita

Infection and Immunity, September 2006, p. 5261-5271, Vol. 74, No. 9
0019-9567/06/$08.00+0     doi:10.1128/IAI.01094-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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