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Innate immune memory after brain injury drives inflammatory cardiac dysfunction [snATAC-seq]

ABSTRACT: Innate immune memory after brain injury drives inflammatory cardiac dysfunction [snATAC-seq]

PROVIDER: PRJNA962132 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24318075_1.fastq.gz	Fastqsanger.gz
	SRR24318075_2.fastq.gz	Fastqsanger.gz
	SRR24318076_1.fastq.gz	Fastqsanger.gz
	SRR24318076_2.fastq.gz	Fastqsanger.gz
	SRR24318077_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Innate immune memory after brain injury drives inflammatory cardiac dysfunction [snATAC-seq]

Project description:Besides the local inflammatory immune response in the brain, stroke also alters systemic immunity. Within the acute and sub-acute phase, the systemic immune response to stroke has been described in detail over last decades. The long-term systemic immunological consequences after stroke are however still elusive. Therefore, a better understanding of these long-lasting chronic effects of stroke on systemic immunity and its impact on remote organ function and secondary comorbidities is needed. Here, we used single-cell RNA sequencing (scRNA-Seq) to investigate the chronic effect of stroke on the transcriptomic signatures of resident myeloid immune cells in various peripheral organs remote from the brain, including the lung, heart, liver, spleen, blood and bone marrow. We observed that monocytes in peripheral organs and in the bone marrow adopt a pro-inflammatory phenotype which persists chronically after stroke. Moreover, the pro-inflammatory profile of monocytes in the bone marrow was transmissible by BM transplantation to naïve recipients, indicating potentially epigenetically imprinted chronic innate immune memory after stroke. Indeed, by performing single-nuclei ATAC sequencing, we found that post-stroke myeloid immune memory after stroke is likely mediated by IL-1b-driven mechanisms, and that neutralization of the post-stroke increase in circulating IL-1b prevented myeloid immune memory.

2024-07-22 | GSE230692 | GEO

Innate immune memory after brain injury drives inflammatory cardiac dysfunction

Project description:Innate immune memory after brain injury drives inflammatory cardiac dysfunction

| PRJNA970816 | ENA

Innate immune memory after brain injury drives inflammatory cardiac dysfunction [BMT2]

Project description:Innate immune memory after brain injury drives inflammatory cardiac dysfunction [BMT2]

| PRJNA1092621 | ENA

Innate immune memory after brain injury drives inflammatory cardiac dysfunction II

Project description:Innate immune memory after brain injury drives inflammatory cardiac dysfunction II

| PRJNA972710 | ENA

Innate immune memory after brain injury drives inflammatory cardiac dysfunction (cardiac interstitial cells)

Project description:Innate immune memory after brain injury drives inflammatory cardiac dysfunction (cardiac interstitial cells)

| PRJNA1095486 | ENA

Innate immune memory after brain injury drives inflammatory cardiac dysfunction [ATAC-Seq]

Project description:Innate immune memory after brain injury drives inflammatory cardiac dysfunction [ATAC-Seq]

| PRJNA1100971 | ENA

Innate immune memory after brain injury drives inflammatory cardiac dysfunction [CUT&tag]

Project description:Innate immune memory after brain injury drives inflammatory cardiac dysfunction [CUT&tag]

| PRJNA1102377 | ENA

Innate immune memory after brain injury drives inflammatory cardiac dysfunction [ATAC-Seq]

Project description:The enormous medical burden of stroke is not only due to the brain injury itself and the acute systemic effects, but is largely determined by chronic comorbidities that develop secondarily after stroke. We hypothesized that the high rate of comorbidity developing after a stroke might have a shared immunological cause, however, the chronic effects of brain injury on systemic immunity have so far been barely investigated. Here, we identified myeloid innate immune memory as a cause of remote organ dysfunction after stroke. Using single-cell sequencing, we identified persistent pro-inflammatory transcriptomic changes in resident monocytes/macrophages in multiple organs one month after experimental ischemic brain injury, which was particularly abundant in the heart and associated with the development of cardiac fibrosis and diastolic dysfunction. A similar phenotype was seen in myocardial autopsy samples from stroke versus control patients. We observed chronic functional changes in myeloid hematopoiesis driven by post-stroke IL-1-mediated epigenetic changes. These alterations could be transplanted to naïve recipient mice and were sufficient to induce cardiac dysfunction. By effectively blocking the trafficking of pro-inflammatory monocytes from the bone marrow to the heart using a dual CCR2/5 inhibitor, we successfully prevented post-stroke cardiac dysfunction. This approach holds promising potential as a novel immune-targeted secondary prevention therapy. We anticipate that the epigenetic immune reprogramming mechanisms detailed here for the brain-heart axis could be generalized to provide a novel framework for explaining the development of various comorbidities after acute tissue injury in remote organs.

2024-07-22 | GSE264093 | GEO