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Peterson, A. L.

Publications and source records attributed to Peterson, A. L..

2 recordsLinked to original sources

Moderate-term dimethyl fumarate treatment reduces pathology of dystrophic skeletal and cardiac muscle in a mouse model

In Duchenne muscular dystrophy (DMD), corticosteroids significantly slow disease progression and have been used as a standard of care tool for more than 30 years. However, corticosteroids also impart side effects severe enough to preclude use in some patients. There remains an unmet need for new therapeutics that target the flow-on pathogenic mechanisms of DMD with a more favourable side-effect profile. We have previously demonstrated that short-term treatment with dual-purpose anti-inflammatory, anti-oxidative dimethyl fumarate (DMF), a drug with indication and established safety data in Multiple Sclerosis, more selectively modulates Duchenne (mdx) immunology than the frequently used corticosteroid, prednisone (PRED). Here, we assess the effect of moderate-term DMF treatment over 5 weeks in the typically mild mdx mouse model that we aggravated using exercise. We show that like PRED, DMF maintains anti-inflammatory action but with additional anti-fibrotic and anti-lipogenic effects on muscle with moderate-term use. This study supports our previous work highlighting DMF as a possible repurposing candidate for DMD, especially for patients who cannot tolerate chronic corticosteroid treatment.

pathology↗

KatG inactivation generates vulnerabilities in isoniazid resistant strains of Mycobacterium tuberculosis

Drug-resistant strains of Mycobacterium tuberculosis are a major global health problem. Resistance to the front-line antibiotic isoniazid is often associated with mutations in the katG encoded bifunctional catalase-peroxidase. We hypothesised that perturbed KatG activity would generate collateral vulnerabilities in INH-resistant katG mutants, providing new pathways to combat isoniazid resistance. Here, we used whole genome CRISPRi screens, transcriptomics, and metabolomics to generate a genome-wide map of cellular vulnerabilities in a M. tuberculosis katG mutant. We discovered that metabolic and transcriptional remodelling compensates for the loss of KatG but in doing so generates vulnerabilities in ribosome biogenesis, and nucleotide and amino acid metabolism. These vulnerabilities were more sensitive to inhibition in an isoniazid-resistant katG mutant under in vitro and host-relevant conditions and translated to clinical populations. These findings provide an experimental framework for developing novel strategies to combat antimicrobial resistance in M. tuberculosis and other bacterial pathogens.

microbiology↗