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Lefamulin: A Novel Pleuromutilin Effective Against Mycobacterium tuberculosis via Efflux Inhibition

ABSTRACT: Lefamulin: A Novel Pleuromutilin Effective Against Mycobacterium tuberculosis via Efflux Inhibition

PROVIDER: PRJNA1180913 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31190388_1.fastq.gz	Fastqsanger.gz
	SRR31190388_2.fastq.gz	Fastqsanger.gz
	SRR31190389_1.fastq.gz	Fastqsanger.gz
	SRR31190389_2.fastq.gz	Fastqsanger.gz
	SRR31190390_1.fastq.gz	Fastqsanger.gz

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Lefamulin: A Novel Pleuromutilin Effective Against Mycobacterium tuberculosis via Efflux Inhibition

Project description:Tuberculosis (TB) remains a major global health challenge, exacerbated by the increasing prevalence of drug-resistant strains. Drug repurposing is a crucial strategy for TB control, particularly in combating resistance. Through this approach, the anti-TB potential of lefamulin was identified as a candidate for systemic administration. Lefamulin demonstrates potent inhibitory activity against Mycobacterium tuberculosis (M.tb) in vitro , in vivo, and within intracellular environments. Notably, it exhibits synergistic effects when combined with the first-line anti-TB drugs rifampicin and isoniazid, as demonstrated in insect model.

2025-06-04 | GSE280850 | GEO

Pleuromutilin Antibiotics Suppress Hepatocellular Carcinoma Growth

Project description:Pleuromutilin antibiotics(Lefamulin, Tiamulin, et al) has application potential in malignancies treatment. To mechanistically investigate the inhibitory activity against HCC of Lefamulin and Tiamulin, we treated Hepa1-6 cells with 37 μg/ml Lefamulin or Tiamulin for 2 days. Then the total RNA was performed RNA-Seq analysis.

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Unveiling the response of efflux pump genes to delamanid in Mycobacterium tuberculosis H37Rv: transcriptomic analysis.

Project description:Efflux pump overexpression is associated with drug resistance in Mycobacterium tuberculosis, but its role in delamanid resistance is not well understood. This study sought to identify efflux pump genes affected by delamanid exposure using transcriptomic analysis. Cultures of M. tuberculosis H37Rv were exposed to delamanid at a sub-inhibitory concentration of ½ MIC for 24 hours, and transcriptomic sequencing was conducted on both treated and untreated samples. Differentially expressed genes (DEGs) were annotated using the UniProt database. The analysis revealed significant upregulation of 23 efflux pump genes under delamanid stress, with 73.9% belonging to the ABC family, 17.39% to the RND family, and 8.69% to the MFS superfamily. These results highlight efflux pump genes that are responsive to sub-inhibitory levels of delamanid.

2026-04-30 | GSE287913 | GEO

A novel TetR-like transcriptional regulator is induced in acid-nitrosative stress and controls expression of an efflux pump in mycobacteria

Project description:Mycobacterium tuberculosis has the ability to survive inside macrophages under acid-nitrosative stress. M. tuberculosis Rv1685c and its orthologue in M. smegmatis, MSMEG_3765, are induced on exposure to acid-nitrosative stress. Both genes are annotated as TetR transcriptional regulators, a family of proteins that regulate a wide range of cellular activities, including multidrug resistance, carbon catabolism and virulence. Here we demonstrate that MSMEG_3765 is co-transcribed with the upstream genes MSMEG_3762 and MSMEG_3763, encoding efflux pump components. RTq-PCR and GFP-reporter assays showed that the MSMEG_3762/63/65 gene cluster, and the orthologous region in M. tuberculosis (Rv1687c/86c/85c), was up-regulated in a MSMEG_3765 null mutant, suggesting that MSMEG_3765 acts as a repressor, typical of this family of regulators. We further defined the MSMEG_3765 regulon using genome-wide transcriptional profiling and confirmed that the MSMEG_3762/63/65 promoter is induced under acid-nitrosative stress. A putative 36 bp regulatory motif was identified upstream of the gene clusters in both M. smegmatis and M. tuberculosis and purified recombinant MSMEG_3765 protein was found to bind to DNA fragments containing this motif from both M. smegmatis and M. tuberculosis upstream regulatory regions. These results suggest that the TetR repressor MSMEG_3765/Rv1685c controls expression of an efflux pump with an, as yet, undefined role in the mycobacterial response to acid-nitrosative stress.

2017-10-24 | E-MTAB-5869 | biostudies-arrayexpress

Exploring proteomic change of intracellular Mycobacterium tuberculosis in response to the Apt-PEGNio/EEP

Project description:The challenge in treating tuberculosis (TB) associated with drug resistance and toxicity drives the efforts in the development of alternative strategies to combat Mycobacterium tuberculosis (Mtb), a major causative pathogen in humans. Propolis extract is considered a promising therapeutic agent since the findings on its effective functions against Mtb.

2025-11-26 | PXD058274 | JPOST Repository

Mycobacterium tuberculosis

Project description:Efflux pumps: Mycobacterium tuberculosis

| PRJNA1013486 | ENA

Transcriptomic Profiling of Efflux Pump Genes in Mycobacterium tuberculosis Under Linezolid Stress

Project description:In this study, we investigated the role of efflux pump genes in linezolid resistance. M. tuberculosis H37Rv cultures were exposed to sub-inhibitory concentrations of linezolid (¼ MIC) for 24 hours, and transcriptomic analysis was performed to identify upregulated genes. Of the 120 genes involved in cell wall processes, 9/120 (7.5%) were efflux pump genes, primarily belonging to the ATP-binding cassette (ABC), major facilitator superfamily (MFS), resistance nodulation division (RND), and small multidrug resistance (SMR) families. qRT-PCR, performed at 1/2, 1/4 and 1/8 MIC of linezolid, confirmed the RNA-seq results, showing that 8/9 (88.88%) of the efflux pump genes were upregulated at 1/8 MIC of linezolid, indicating that this concentration is optimal for studying efflux pump activity. These findings not only identify 1/8 MIC as optimum concentration for efflux pump studies after linezolid exposure, they also highlight the significant role of efflux pumps in linezolid resistance, providing potential targets for further research on efflux pumps in clinical isolates of M. tuberculosis.

2025-02-20 | GSE288598 | GEO

The cyclic-AMP binding domain of the efflux pump Rv3728 acts as a regulator of phosphatidyl-myo-inositol mannosides composition in Mycobacterium tuberculosis

Project description:Tuberculosis (TB) is an ancient disease caused by the intracellular bacterial pathogen Mycobacterium tuberculosis (Mtb). The rise of antimicrobial resistance (AMR) threatens to bring Mtb to the forefront of bacterial pathogens as the current treatments are increasingly becoming ineffective. Understanding the development of AMR and the virulence processes of Mtb is crucial for the identification of new drug targets and the rational design of anti-TB treatments. One of the established mechanisms of resistance is through the function of efflux proteins, which are transmembrane transporters that bind and remove antibiotic molecules out from the cell. Here, we determine the role of Rv3728, a major facilitator superfamily (MFS) efflux pump protein, which also predicted to bind 3',5'-cyclic adenosine monophosphate (cAMP). Using bioinformatic tools and cAMP binding assay, we confirm that Rv3728 binds to cAMP and identified E597 and R606 as important residues involved in binding. Although Rv3728 deletion has no impact on bacterial resistance and tolerance to different antibiotics, it affects membrane permeability and alters the acylation profile of phosphatidyl-myo-inositol mannosides lipids.

2024-06-10 | GSE268977 | GEO

Transcriptomic Profiling of Efflux Pump Genes in Mycobacterium tuberculosis Under Linezolid Stress

Project description:Transcriptomic Profiling of Efflux Pump Genes in Mycobacterium tuberculosis Under Linezolid Stress

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Mycobacterium tuberulosis H37Rv strains: Control vs. Osthole.

Project description:Transcriptional profiling of Mycobacterium tuberculosis H37Rv strains comparing control DMSO treated strains with Osthole treated strains. Goal was to determine the effects of Osthole against Mycobacterium tuberculosis H37Rv strains.

2011-09-14 | GSE32076 | GEO

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