SecA2 of Mycobacterium tuberculosis contributes to intracellular survival, immune modulation, and surface properties of the bacillus Public Deposited
- Last Modified
- March 21, 2019
- Creator
-
Kurtz, Sherry Lynn
- Affiliation: School of Medicine, Department of Microbiology and Immunology
- Abstract
- SecA2 is part of a specialized protein export pathway of Mycobacterium tuberculosis that is important to virulence. We present evidence that a ΔsecA2 mutant of M. tuberculosis is defective for replication in macrophages. In addition, macrophages infected with the ΔsecA2 mutant produce more proinflammatory TNF-α, IL-6, and RNI than those infected with wild type M. tuberculosis. These host factors are induced by M. tuberculosis through TLR/MyD88 signaling pathways. The attenuated phenotype of the ΔsecA2 mutant in macrophages was dependent on the signaling adaptor MyD88 and TNF-α. Our data suggests that the role of SecA2 in virulence is to export factors which limit the host immune response, and thereby protects the bacillus against MyD88/TNF-α dependent defenses. Finally, we reveal a role for SecA2 in assembling the cell surface structure of M. tuberculosis, a finding that may have implications on the biology of the organism, and pathogenesis.
- Date of publication
- December 2007
- DOI
- Resource type
- Rights statement
- In Copyright
- Advisor
- Braunstein, Miriam
- Degree granting institution
- University of North Carolina at Chapel Hill
- Language
- Access
- Open access
- Parents:
This work has no parents.
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SecA2 of Mycobacterium tuberculosis contributes to intracellular survival, immune modulation, and surface properties of the bacillus | 2019-04-11 | Public |
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