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Infection and Immunity, April 2004, p. 2400-2404, Vol. 72, No. 4
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.4.2400-2404.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

MyD88-Deficient Mice Display a Profound Loss in Resistance to Mycobacterium tuberculosis Associated with Partially Impaired Th1 Cytokine and Nitric Oxide Synthase 2 Expression

Charles A. Scanga,1* Andre Bafica,1 Carl G. Feng,1 Allen W. Cheever,2 Sara Hieny,1 and Alan Sher1

Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892,1 Biomedical Research Institute, Rockville, Maryland 208522

Received 22 December 2003/ Accepted 13 January 2004

Mycobacterium tuberculosis possesses agonists for several Toll-like receptors (TLRs), yet mice with single TLR deletions are resistant to acute tuberculosis. MyD88-/- mice were used to examine whether TLRs play any role in protection against aerogenic M. tuberculosis H37Rv infection. MyD88-/- mice failed to control mycobacterial replication and rapidly succumbed. Moreover, expressions of interleukin 12, tumor necrosis factor alpha, gamma interferon, and nitric oxide synthase 2 were markedly decreased in the knockout animals. These results argue that resistance to M. tuberculosis must depend on MyD88-dependent signals mediated by an as-yet-undetermined TLR or a combination of TLRs.

* Corresponding author. Mailing address: Building 50, Room 6148, 50 South Dr., Bethesda, MD 20892-8003. Phone: (301) 594-3454. Fax: (301) 402-0890. E-mail: cscanga{at}niaid.nih.gov.

Editor: J. F. Urban, Jr.

Infection and Immunity, April 2004, p. 2400-2404, Vol. 72, No. 4
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.4.2400-2404.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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