Abstract
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.
MeSH terms
-
Adaptor Proteins, Signal Transducing
-
Animals
-
Antigens, Differentiation / genetics
-
Antigens, Differentiation / physiology*
-
Cytokines / biosynthesis
-
Lung / microbiology
-
Lung / pathology
-
Mice
-
Mice, Inbred C57BL
-
Mice, Knockout
-
Mycobacterium tuberculosis / immunology*
-
Mycobacterium tuberculosis / pathogenicity
-
Myeloid Differentiation Factor 88
-
Nitric Oxide Synthase / metabolism*
-
Receptors, Immunologic / genetics
-
Receptors, Immunologic / physiology*
-
Th1 Cells / immunology
-
Th1 Cells / pathology*
-
Tuberculosis, Pulmonary / immunology*
-
Tuberculosis, Pulmonary / mortality
-
Tuberculosis, Pulmonary / pathology
-
Virulence
Substances
-
Adaptor Proteins, Signal Transducing
-
Antigens, Differentiation
-
Cytokines
-
Myd88 protein, mouse
-
Myeloid Differentiation Factor 88
-
Receptors, Immunologic
-
Nitric Oxide Synthase