原创力文档a novel in vitro multiple-stress dormancy model for mycobacterium tuberculosis generates a lipid-loaded, drug-tolerant, dormant pathogen一种新的体外multiple-stress结核分枝杆菌休眠模式生成一个lipid-loaded,drug-tolerant,休眠病原体.pdfVIP
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a novel in vitro multiple-stress dormancy model for mycobacterium tuberculosis generates a lipid-loaded, drug-tolerant, dormant pathogen一种新的体外multiple-stress结核分枝杆菌休眠模式生成一个lipid-loaded,drug-tolerant,休眠病原体
A Novel In Vitro Multiple-Stress Dormancy Model for
Mycobacterium tuberculosis Generates a Lipid-Loaded,
Drug-Tolerant, Dormant Pathogen
Chirajyoti Deb, Chang-Muk Lee, Vinod S. Dubey, Jaiyanth Daniel, Bassam Abomoelak, Tatiana D.
Sirakova, Santosh Pawar, Linda Rogers, Pappachan E. Kolattukudy*
Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, United States of America
Abstract
Background: Mycobacterium tuberculosis (Mtb) becomes dormant and phenotypically drug resistant when it encounters
multiple stresses within the host. Inability of currently available drugs to kill latent Mtb is a major impediment to curing and
possibly eradicating tuberculosis (TB). Most in vitro dormancy models, using single stress factors, fail to generate a truly
dormant Mtb population. An in vitro model that generates truly dormant Mtb cells is needed to elucidate the metabolic
requirements that allow Mtb to successfully go through dormancy, identify new drug targets, and to screen drug candidates
to discover novel drugs that can kill dormant pathogen.
Methodology/Principal Findings: We developed a novel in vitro multiple-stress dormancy model for Mtb by applying
combined stresses of low oxygen (5%), high CO2 (10%), low nutrient (10% Dubos medium) and acidic pH (5.0), conditions
Mtb is thought to encounter in the host. Under this condition, Mtb stopped replicating, lost acid-fastness, accumulated
triacylglycerol (TG) and wax ester (WE), and concomitantly acquired phenotypic antibiotic-resistance. Putative neutral lipid
biosynthetic genes were up-regulated. These genes may serve as potential targets for new antilatency drugs. The
triacylglycerol synthase1 (tgs1) deletion mutant, with impaired ability to accumulate TG, exhibited a lesser degree of
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