Antimicrobial Treatment Improves Mycobacterial Survival in Nonpermissive Growth Conditions | Zendy

Obolbek Turapov | Zendy; Simon J. Waddell | Zendy; B. F. Burke | Zendy; Sarah Glenn | Zendy; Asel A. Sarybaeva | Zendy; Griselda Tudó | Zendy; Gilles Labesse | Zendy; Danielle I. Young | Zendy; Michael Young | Zendy; Peter W. Andrew | Zendy; Philip D. Butcher | Zendy; Martin CohenGonsaud | Zendy; Galina V. Mukamolova | Zendy

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Antimicrobial Treatment Improves Mycobacterial Survival in Nonpermissive Growth Conditions

Author(s) -

Obolbek Turapov,

Simon J. Waddell,

B. F. Burke,

Sarah Glenn,

Asel A. Sarybaeva,

Griselda Tudó,

Gilles Labesse,

Danielle I. Young,

Michael Young,

Peter W. Andrew,

Philip D. Butcher,

Martin CohenGonsaud,

Galina V. Mukamolova

Publication year - 2014

Publication title -

antimicrobial agents and chemotherapy

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.07

H-Index - 259

eISSN - 1070-6283

pISSN - 0066-4804

DOI - 10.1128/aac.02774-13

Subject(s) - antimicrobial , microbiology and biotechnology , regulator , biology , mycobacterium tuberculosis , multidrug tolerance , bacteria , efflux , tuberculosis , bacilli , in vitro , mycobacterium , mycobacterium bovis , antibiotics , biofilm , medicine , gene , genetics , pathology

Antimicrobials targeting cell wall biosynthesis are generally considered inactive against nonreplicating bacteria. Paradoxically, we found that under nonpermissive growth conditions, exposure of Mycobacterium bovis BCG bacilli to such antimicrobials enhanced their survival. We identified a transcriptional regulator, RaaS (for regulator of antimicrobial-assisted survival), encoded by bcg1279 (rv1219c) as being responsible for the observed phenomenon. Induction of this transcriptional regulator resulted in reduced expression of specific ATP-dependent efflux pumps and promoted long-term survival of mycobacteria, while its deletion accelerated bacterial death under nonpermissive growth conditions in vitro and during macrophage or mouse infection. These findings have implications for the design of antimicrobial drug combination therapies for persistent infectious diseases, such as tuberculosis.

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