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The sigma factor E of Mycobacterium tuberculosis modulates the inflammatory response of macrophages

ABSTRACT: Mycobacterium tuberculosis (Mtb) is well adapted to survive in macrophages and usually subverts the bactericidal mechanisms of these professional phagocytes. The adaptation of Mtb to the intracellular life depends on its ability to regulate the expression of its genes. Among the most important bacterial transcription activators are the sigma factors that bind to the RNA polymerase and give it promotor specificity. Sigma factor E (SigE) controls the expression of genes that are essential for Mtb virulence. Analysis of the macrophage transcriptional response indicated that proteins encoded by the sigE regulon are involved in the modulation of the macrophage inflammatory response. We compared the global gene expression of mouse bone marrow macrofages infected with H37Rv and SigE to the gene expression profile of the uninfected macrophages.

ORGANISM(S): Mus musculus

SUBMITTER: Analia Trevani

PROVIDER: E-GEOD-7871 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The sigma factor E of Mycobacterium tuberculosis modulates the inflammatory response of human THP1 cells

Project description:Mycobacterium tuberculosis (Mtb) is well adapted to survive in macrophages and usually subverts the bactericidal mechanisms of these professional phagocytes. The adaptation of Mtb to the intracellular life depends on its ability to regulate the expression of its genes. Among the most important bacterial transcription activators are the sigma factors that bind to the RNA polymerase and give it promotor specificity. Sigma factor E (SigE) controls the expression of genes that are essential for Mtb virulence. Analysis of the macrophage transcriptional response indicated that proteins encoded by the sigE regulon are involved in the modulation of the macrophage inflammatory response. We compared the global gene expression of THP1 macrophages infected with H37Rv and SigE to the gene expression profile of uninfected macrophages.

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