SecA2 of Mycobacterium tuberculosis contributes to intracellular survival, immune modulation, and surface properties of the bacillus Public Deposited

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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.
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  • In Copyright
Advisor
  • Braunstein, Miriam
Degree granting institution
  • University of North Carolina at Chapel Hill
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  • Open access
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SecA2 of Mycobacterium tuberculosis contributes to intracellular survival, immune modulation, and surface properties of the bacillus 2019-04-11 Public