Aloe Emodin Reduces Phthiodiolone Dimycocerosate Potentiating Vancomycin Susceptibility on Mycobacteria |
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Authors: | Céline Rens Pieter-Jan Ceyssens Françoise Laval Philippe Lefèvre Vanessa Mathys Mamadou Daffé Véronique Fontaine |
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Institution: | 1.Unit of Pharmaceutical Microbiology and Hygiene,Université Libre de Bruxelles (ULB),Brussels,Belgium;2.NRC Mycobacteria and Tuberculosis,Scientific Institute of Public Health,Brussels,Belgium;3.Department of “Tuberculosis and Infection Biology”, Institute of Pharmacology and Structural Biology,University of Toulouse, CNRS, University Paul Sabatier, UMR 5089,Toulouse Cedex 04,France |
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Abstract: | Treatment of tuberculosis still represent a major public health issue. The emergence of multi-and extensively-drug resistant (MDR and XDR) Mycobacterium tuberculosis clinical strains further pinpoint the urgent need for new anti-tuberculous drugs. We previously showed that vancomycin can target mycobacteria lacking cell wall integrity, especially those lacking related phthiocerol and phthiodolone dimycocerosates, PDIM A and PDIM B, respectively. As aloe emodin was previously hypothesized to be able to target the synthesis of mycobacterial cell wall lipids, we tested its ability to potentiate glycopeptides antimycobacterial activity. The aloe emodin with the vancomycin induced a combination effect beyond simple addition, close to synergism, at a concentration lower to reported IC50 cytotoxic value, on M. bovis BCG and on H37Rv M. tuberculosis. Interestingly, out of six MDR and pre-XDR clinical strains, one showed a strong synergic susceptibility to the drug combination. Mycobacterial cell wall lipid analyses highlighted a selective reduction of PDIM B by aloe emodin. |
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