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Biology subjects

Weiner, D. M.

Publications and source records attributed to Weiner, D. M..

2 recordsLinked to original sources

In vitro dormancy models improve ability to predict treatment response in severe marmoset tuberculosis lesions

Tuberculosis lesions are structurally and physiologically heterogeneous, creating microenvironments that restrict antibiotic penetration and alter bacterial susceptibility. This heterogeneity remains a major impediment to shortening tuberculosis treatment, as it is difficult to predict which regimens will sterilize bacteria in these hard-to-treat lesion niches. Many in vitro systems and commonly used animal models fail to recapitulate the necrotic, caseous lesion pathology associated with treatment failure and relapse. Here, we show that resource-efficient in vitro assays engineered to mimic key lesion microenvironments, including those with lipid-rich, caseum-like matrices with controlled oxygenation and pH, generate drug-response metrics that predict lesion-level treatment responses in a non-human primate model. We stratified individual marmoset lesions by baseline 2-deoxy-2-[18F] fluoro-D-glucose ([18F] FDG) positron emission tomography/computed tomography (PET/CT) features, then quantified drug potency and interactions across three lipid-induced dormancy (LIDs) conditions under both equipotent and lesion pharmacokinetic-informed dosing schemes. LIDs-based and pharmacokinetic-informed measurements aligned more closely with treatment responses in severe lesions than conventional in vitro data and recapitulated interaction patterns consistent with known regimen performance. Integrating imaging-derived and in vitro features in multivariate, sequential computational models improved predictive accuracy over baseline imaging alone and identified a subset of informative in vitro metrics. Together, these results establish a scalable framework linking lesion-mimicking assays to lesion-specific outcomes, enabling earlier, more cost-effective prioritization of pre-clinical regimens aimed at sterilizing hard-to-treat tuberculosis lesions and shortening therapy.

molecular biology↗

Distributable, Metabolic PET Reporting of Tuberculosis

Tuberculosis remains a large global disease burden for which treatment regimens are protracted and monitoring of disease activity difficult. Existing detection methods rely almost exclusively on bacterial culture from sputum which limits sampling to organisms on the pulmonary surface. Advances in monitoring tuberculous lesions have utilized the common glucoside [18F]FDG, yet lack specificity to the causative pathogen Mycobacterium tuberculosis (Mtb) and so do not directly correlate with pathogen viability. Here we show that a close mimic that is also positron-emitting of the non-mammalian Mtb disaccharide trehalose - 2-[18F]fluoro-2-deoxytrehalose ([18F]FDT) - can act as a mechanism-based enzyme reporter in vivo. Use of [18F]FDT in the imaging of Mtb in diverse models of disease, including non-human primates, successfully co-opts Mtb-specific processing of trehalose to allow the specific imaging of TB-associated lesions and to monitor the effects of treatment. A pyrogen-free, direct enzyme-catalyzed process for its radiochemical synthesis allows the ready production of [18F]FDT from the most globally-abundant organic 18F-containing molecule, [18F]FDG. The full, pre-clinical validation of both production method and [18F]FDT now creates a new, bacterium-specific, clinical diagnostic candidate. We anticipate that this distributable technology to generate clinical-grade [18F]FDT directly from the widely-available clinical reagent [18F]FDG, without need for either bespoke radioisotope generation or specialist chemical methods and/or facilities, could now usher in global, democratized access to a TB-specific PET tracer.

biochemistry↗