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

• https://doi.org/10.17615/d0wx-y415

Resource type

• Masters Thesis

Rights statement

• In Copyright

Advisor

• Braunstein, Miriam

Degree granting institution

• University of North Carolina at Chapel Hill

Language

• English

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	Press to Select an action Download