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Clinical and Vaccine Immunology, August 2008, p. 1248-1258, Vol. 15, No. 8
1071-412X/08/$08.00+0     doi:10.1128/CVI.00019-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Influence of Mycobacterium bovis BCG Vaccination on Cellular Immune Response of Guinea Pigs Challenged with Mycobacterium tuberculosis

Diane Ordway,^* Marcela Henao-Tamayo, Crystal Shanley, Erin E. Smith, Gopinath Palanisamy, Baolin Wang, Randall J. Basaraba, and Ian M. Orme

Mycobacteria Research Laboratories, Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado 80523

Received 15 January 2008/ Returned for modification 19 March 2008/ Accepted 20 May 2008

Mycobacterium bovis bacillus Calmette-Guérin (BCG) currently remains the only licensed vaccine for the prevention of tuberculosis. In this study, we used a newly described flow cytometric technique to monitor changes in cell populations accumulating in the lungs and lymph nodes of naïve and vaccinated guinea pigs challenged by low-dose aerosol infection with virulent Mycobacterium tuberculosis. As anticipated, vaccinated guinea pigs controlled the growth of the challenge infection more efficiently than controls did. This early phase of bacterial control in immune animals was associated with increased accumulation of CD4 and CD8 T cells, including cells expressing the activation marker CD45, as well as macrophages expressing class II major histocompatibility complex molecules. As the infection continued, the numbers of T cells in the lungs of vaccinated animals waned, whereas the numbers of these cells expressing CD45 increased. Whereas BCG vaccination reduced the influx of heterophils (neutrophils) into the lungs, an early B-cell influx was observed in these vaccinated animals. Overall, vaccine protection was associated with reduced pathology and lung damage in the vaccinated animals. These data provide the first direct evidence that BCG vaccination accelerates the influx of protective T-cell and macrophage populations into the infected lungs, diminishes the accumulation of nonprotective cell populations, and reduces the severity of lung pathology.

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* Corresponding author. Mailing address: Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523-1682. Phone: (970) 491-7469. Fax: (970) 491-5129. E-mail: D.Ordway-Rodriguez{at}colostate.edu

Published ahead of print on 28 May 2008.

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Clinical and Vaccine Immunology, August 2008, p. 1248-1258, Vol. 15, No. 8
1071-412X/08/$08.00+0     doi:10.1128/CVI.00019-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

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