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Infection and Immunity, September 2003, p. 5266-5272, Vol. 71, No. 9
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.9.5266-5272.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

SWR Mice Are Highly Susceptible to Pulmonary Infection with Mycobacterium tuberculosis

Oliver C. Turner,1 Robert G. Keefe,1 Isamu Sugawara,2 Hiroyuki Yamada,2 and Ian M. Orme1*

Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado 80523,1 The Research Institute of Tuberculosis, Matsuyama, Kiyose, Tokyo, Japan2

Received 3 January 2003/ Returned for modification 18 February 2003/ Accepted 5 June 2003

Inbred mice differ in their abilities to control the growth of Mycobacterium tuberculosis in the lung and can as a result be regarded as either resistant or susceptible strains. In this study we report that the SWR mouse is both highly susceptible and in addition appears incapable of establishing a characteristic state of chronic disease after low-dose aerosol infection. In comparison to C57BL/6 mice, SWR mice were unable to contain the bacterial load in the lungs, resulting in progressive fatal disease. Histologic analysis of the lung tissue revealed evidence of a florid inflammatory cell response in the SWR mice leading to degeneration and necrosis and consolidation of a large percentage of the lung surface area. Digestion of infected lungs and analysis by flow cytometry demonstrated an initially similar but eventually higher number of lymphocytes accumulating in the SWR mice. Additionally, in contrast to the C57BL/6 mice, SWR mice had a significantly lower percentage of CD4 T cells in the lungs showing evidence of proliferation and positive intracellular staining for gamma interferon during the first two months of infection, and a lower percentage of both CD4 and CD8T cells exhibiting differentiation to an effector/memory phenotype during the first month of infection. We propose that further investigation of the SWR mouse may provide a new animal model for immunocompetent individuals apparently unable to effectively control the growth of M. tuberculosis in the lung.

* Corresponding author. Mailing address: Department of Microbiology, Immunology and Pathology, Fort Collins, CO 80523. Phone: (970) 491-5777. Fax: (970) 491-5125. E-mail: iorme{at}lamar.colostate.edu.

Editor: S. H. E. Kaufmann

Infection and Immunity, September 2003, p. 5266-5272, Vol. 71, No. 9
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.9.5266-5272.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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