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Azithromycin promotes relapse by disrupting immune and metabolic networks after allogeneic stem cell transplantation

ABSTRACT: Azithromycin promotes relapse by disrupting immune and metabolic networks after allogeneic stem cell transplantation

PROVIDER: PRJNA811516 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18184200_1.fastq.gz	Fastqsanger.gz
	SRR18184200_2.fastq.gz	Fastqsanger.gz
	SRR18184201_1.fastq.gz	Fastqsanger.gz
	SRR18184201_2.fastq.gz	Fastqsanger.gz
	SRR18184202_1.fastq.gz	Fastqsanger.gz

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Azithromycin promotes relapse by disrupting immune and metabolic networks after allogeneic stem cell transplantation

Project description:Administration of azithromycin after allogeneic hematopoietic stem cell transplantation for hematological malignancies has been associated with relapse in a randomized phase 3 controlled clinical trial. Studying 240 samples from patients randomized in this trial is a unique opportunity to better understand the mechanisms underlying relapse, the first cause of mortality after transplantation. We used multi-omics on patients' samples to decipher immune alterations associated with azithromycin intake and post-transplant relapsed malignancies. Azithromycin was associated with a network of altered energy metabolism pathways and immune subsets, including T cells biased toward immunomodulatory and exhausted profiles. In vitro, azithromycin exposure inhibited T cells cytotoxicity against tumor cells and impaired T cells metabolism through glycolysis inhibition, mitochondrial genes downregulation, and immunomodulatory genes upregulation, notably SOCS1. These results highlight that azithromycin directly affects immune cells that favor relapse, which raises caution about long-term use of azithromycin treatment in patients at high risk of malignancies.

2022-08-22 | MTBLS406 | MetaboLights

Azithromycin promotes relapse by disrupting immune and metabolic networks after allogeneic stem cell transplantation

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Azithromycin promotes relapse by disrupting immune and metabolic networks after allogeneic stem cell transplantation

Project description:The aim of this experiment was to identify gene expression changes in sorted T cells from healthy donors two days after CD3/CD28 activation in the presence of azithromycin or a control. Following cell clustering according to their phenotype, gene expression was compared between azithromycin treated and non-treated activated T cells. We identified a downregulation in mitochondrial genes expression and pro-inflammatory genes and upregulation of anti-inflammatory genes such as SOCS1.

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Azithromycin promotes relapse by disrupting immune and metabolic networks after allogeneic stem cell transplantation

Project description:The aim of this experiment was to identify gene expression changes in patients's PBMC from ALLOZITHRO's study cohorte. Following cell clustering according to their phenotype, gene expression was compared between azithromycin treated PBMC's patients and non-treated PBMC. We identified a downregulation in several pathways such as mTOR, JAK-STAT, NF B, mitochondrial functions and inflammatory response.

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Project description:Allogeneic stem cell transplantation is used widely in the treatment of hematopoietic malignancy. However relapse of malignant disease is the primary cause of treatment failure and reflects loss of the immunological graft versus leukaemia effect. We studied the transcriptional and phenotypic profile of CD8+ T cells in the first month following transplantation and related this to risk of subsequent relapse. Single cell transcriptional profiling identified 5 discrete CD8+ T cell clusters. High levels of T cell activation and acquisition of a regulatory transcriptome were apparent in patients who went on to suffer disease relapse. A relapse-associated gene signature of 39 genes was then assessed in a confirmation cohort of 34 patients. High level expression of the inhibitory receptor CD94/NKG2A on CD8+ T cells within the first month was associated with 4.8 fold increased risk of relapse and 2.7 fold reduction in survival over the subsequent 4 years. Furthermore, reduced expression of the activatory molecule CD96 was associated with 2.2 fold increased risk of relapse and 1.9 fold reduction in survival. This work identifies CD94 and CD96 as potential targets for CD8-directed immunotherapy in the very early phase following allogeneic transplantation with the potential to reduce long term relapse rates and improve patient survival.

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