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© Giulia Manina, Institut Pasteur
Mycobacterium tuberculosis dual fluorescent reporter of metabolic activity. Green (active bacilli) and red fluorescence (quiescent bacilli) are merged, 100X magnification.
Publication : Tuberculosis (Edinburgh, Scotland)

Azole resistance in Mycobacterium tuberculosis is mediated by the MmpS5-MmpL5 efflux system

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Tuberculosis (Edinburgh, Scotland) - 11 Oct 2008

Milano A, Pasca MR, Provvedi R, Lucarelli AP, Manina G, Ribeiro AL, Manganelli R, Riccardi G

Link to Pubmed [PMID] – 18851927

Tuberculosis (Edinb) 2009 Jan;89(1):84-90

Tuberculosis (TB) remains the leading cause of mortality due to a bacterial pathogen, Mycobacterium tuberculosis. Moreover, the recent isolation of M. tuberculosis strains resistant to both first- and second-line antitubercular drugs (XDR-TB) threatens to make the treatment of this disease extremely difficult and becoming a threat to public health worldwide. Recently, it has been shown that azoles are potent inhibitors of mycobacterial cell growth and have antitubercular activity in mice, thus favoring the hypothesis that these drugs may constitute a novel strategy against tuberculosis disease. To investigate the mechanisms of resistance to azoles in mycobacteria, we isolated and characterized several spontaneous azoles resistant mutants from M. tuberculosis and Mycobacterium bovis BCG. All the analyzed resistant mutants exhibited both increased econazole efflux and increased transcription of mmpS5-mmpL5 genes, encoding a hypothetical efflux system belonging to the resistance-nodulation-division (RND) family of transporters. We found that the up-regulation of mmpS5-mmpL5 genes was linked to mutations either in the Rv0678 gene, hypothesized to be involved in the transcriptional regulation of this efflux system, or in its putative promoter/operator region.

http://www.ncbi.nlm.nih.gov/pubmed/18851927