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Infection and Immunity, December 2005, p. 8369-8380, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.8369-8380.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Mycobacterium-Induced Potentiation of Type 1 Immune Responses and Protection against Malaria Are Host Specific

Kathleen R. Page,1* Anne E. Jedlicka,2 Benjamin Fakheri,4 Gregory S. Noland,2 Anup K. Kesavan,1 Alan L. Scott,2 Nirbhay Kumar,2 and Yukari C. Manabe1,2,3

Department of Medicine, School of Medicine, Johns Hopkins University, Baltimore, Maryland,1 W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland,2 Department of International Health, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland,3 Yeshiva University, New York, New York4

Received 29 June 2005/ Returned for modification 17 August 2005/ Accepted 31 August 2005

Malaria and tuberculosis are endemic in many regions of the world, and coinfection with the two pathogens is common. In this study, we examined the effects of long- and short-term infection with Mycobacterium tuberculosis on the course of a lethal form of murine malaria in resistant (C57BL/6) and susceptible (BALB/c) mice. C57BL/6 mice coinfected with M. tuberculosis CDC1551 and Plasmodium yoelii 17XL had a lower peak parasitemia and increased survival compared to mice infected with P. yoelii 17XL alone. Splenic microarray analysis demonstrated potentiation of type 1 immune responses in coinfected C57BL/6 mice, which was especially prominent 5 days after infection with P. yoelii 17XL. Splenocytes from coinfected C57BL/6 mice produced higher levels of gamma interferon (IFN-{gamma}) and tumor necrosis factor alpha than splenocytes from mice infected with either pathogen alone. Interestingly, mycobacterium-induced protection against lethal P. yoelii is mouse strain specific. BALB/c mice were significantly more susceptible than C57BL/6 mice to infection with P. yoelii 17XL and were not protected against lethal malaria by coinfection with M. tuberculosis. In addition, M. tuberculosis did not augment IFN-{gamma} responses in BALB/c mice subsequently infected with P. yoelii 17XL. These data indicate that M. tuberculosis-induced potentiation of type 1 immune responses is associated with protection against lethal murine malaria.

* Corresponding author. Mailing address: Center for Tuberculosis Research, 1503 E. Jefferson Street, Rm. 108, Baltimore, MD 21231. Phone: (443) 287-0084. Fax: (410) 614-8173. E-mail: kpage2{at}jhmi.edu.

Editor: J. L. Flynn

Infection and Immunity, December 2005, p. 8369-8380, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.8369-8380.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.





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