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Bedaquiline remodels the macrophage response

ABSTRACT: Bedaquiline remodels the macrophage response

PROVIDER: PRJNA550090 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9336560.fastq.gz	Fastqsanger.gz
	SRR9336570.fastq.gz	Fastqsanger.gz
	SRR9336580.fastq.gz	Fastqsanger.gz
	SRR9336561.fastq.gz	Fastqsanger.gz
	SRR9336571.fastq.gz	Fastqsanger.gz

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Bedaquiline remodels the macrophage response

Project description:Background: Infectious diseases are still a leading cause of death and, with the emergence of drug resistance, pose a great threat to human health. New drugs are thus continually being developed, without their effects on the immune system being studied in-depth. Here we aim to evaluate the impact of a recently release anti-TB drug, named bedaquiline (BDQ), on the response of human macrophages infected with Mycobacterium tuberculosis (MTB). Results: Here, we used MTB resistant to BDQ as a model of bacterial infection to examine the impact of BDQ on the human macrophage response. Gene expression profiling has revealed about 1,500 genes differentially expressed in MTB infected macrophages incubated with BDQ. The expression of 499 genes was upregulated and that of 996 downregulated upon treatment. The gene set up-regulated by BDQ was significantly enriched for genes involved in glucose/phospholipid metabolism, lysosome and autophagy. We found similar results with uninfected macrophages-treated with BDQ. Conclusions: Our results highlight the importance to study the interactions between antibiotics and host cells at the molecular level to better understand the consequences of antibiotic treatment during infection

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Transcriptional Response of Mycobacterium tuberculosis H37Rv to Bedaquiline

Project description:Bacteria commonly adapt to stresses by altering gene expression. To understand the response of M. tuberculosis (MTB) to bedaquiline, we performed transcriptomics over a time-course on MTB bacilli exposed to the drug.

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Project description:The ability of Mycobacterium tuberculosis (Mtb) to adopt heterogeneous physiological states, underlies it’s success in evading the immune system and tolerating antibiotic killing. Drug tolerant phenotypes are a major reason why the tuberculosis (TB) mortality rate is so high, with over 1.8 million deaths annually. To develop new TB therapeutics that better treat the infection (faster and more completely), a systems-level approach is needed to reveal the complexity of network-based adaptations of Mtb. Here, we report the transcriptional response of Mtb to the drug Bedaquiline. We performed transcriptomic sequencing (RNA-seq) on Mtb bacilli at 4, 24, 72 h following exposure to the drug.

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Project description:Transcriptional profiling of M. smegmatis mc2155 grown on Hartmans de Bont (HdB) supplemented with 0.2% glycerol and 0.05% Tween80 challenged with 2 μg/ml Bedaquiline and Dimethyl sulfoxide (DMSO) Two-condition experiment. Biological replicates: 5 independently grown and harvested. One replicate per array.

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