4.5 Article

Global transcriptional profiles of Mycobacterium tuberculosis treated with plumbagin

Journal

WORLD JOURNAL OF MICROBIOLOGY & BIOTECHNOLOGY
Volume 27, Issue 10, Pages 2261-2269

Publisher

SPRINGER
DOI: 10.1007/s11274-011-0689-3

Keywords

Antimycobacterial; Plumbagin; Mycobacterium tuberculosis; Microarray

Funding

  1. Important National Science & Technology Specific Projects [2008ZX10301]
  2. Specialized Research Fund for the Doctoral Program of Higher Education (SRFDP) [200801831051]
  3. National Nature Science Foundation of China [30871889]
  4. Fund for Science and Technology Development of the Jilin Province, China [200705233]
  5. Fundamental Research Funds for the Central Universities

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Mycobacterium tuberculosis (M. tuberculosis) remains one of the world's most prevalent and serious pathogens, and multiple resistant strains are increasingly widespread. The recent emergence of multidrug-resistant and extensively drug-resistant (XDR-TB) strains has increased the importance of searching for alternative targets to develop new antimycobacterial drugs. Plumbagin (PL), a natural plant product, has been reported to have potential antimicrobial activity against M. tuberculosis, but the response mechanisms of M. tuberculosis to PL are still poorly understood. In this study, we used a commercial oligonucleotide microarray to determine the overall transcriptional response of M. tuberculosis H37Rv triggered by exposure to subinhibitory concentrations of PL. A total of 274 genes were found to be differentially regulated by PL. Of these, 103 genes were upregulated, and 171 genes were downregulated. A number of important genes were significantly regulated that are involved in various pathways, such as chaperonins, PE/PPE multigene families, and genes involved in the cell envelope, virulence, and 50S ribosomes. To our knowledge, this genome-wide transcriptomics approach has produced the first insights into the response of M. tuberculosis to a PL challenge. These results will pave the way for exploring the mechanisms of PL action against M. tuberculosis.

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