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The role of EZH2 in sepsis-induced acute lung injury [RNA-Seq]

ABSTRACT: The role of EZH2 in sepsis-induced acute lung injury [RNA-Seq]

PROVIDER: PRJNA1123592 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29386084_1.fastq.gz	Fastqsanger.gz
	SRR29386084_2.fastq.gz	Fastqsanger.gz
	SRR29386085_1.fastq.gz	Fastqsanger.gz
	SRR29386085_2.fastq.gz	Fastqsanger.gz
	SRR29386086_1.fastq.gz	Fastqsanger.gz

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The role of EZH2 in sepsis-induced acute lung injury [RNA-Seq]

Project description:To investigate the role of EZH2 in sepsis-induced acute lung injury, we established a mouse model of sepsis in which macrophages specifically knocked out EZH2.We then used RNA-seq data from lung tissues of four groups of mice for gene expression profiling.

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Sepsis-induced acute lung injury is exacerbated by pulmonary Wnt signaling-dependent migration of small intestinal memory γδT17 cells to the lung

Project description:Sepsis, a worldwide health crisis, is notorious for its high mortality rate, often attributed to the development of acute lung injury. In this context, the lung, being particularly vulnerable to septic damage, emerge as a primary battleground. The possible roles of the gut-lung axis mediated by the gut microbiota and its metabolic products in the context of acute lung injury have been documented. However, the direct migration of intestinal immune cells to the lung as a mediator of acute lung injury remains unclear. Our study unveiled a process where cecal ligation and puncture-induced sepsis prompted a migration of γδ T cells from the small intestine to the lung, subsequently triggering an overwhelming inflammatory response dominated by IL-17A. Small intestinal memory γδT17 cells (CD44+ IL-7Rhigh CD8low Ly6C–) were the major subtype of γδ T cells that migrated from the small intestine to the lung and aggravated acute lung injury. Moreover, the activation of the Wnt signaling in the alveolar macrophages during sepsis was identified as a driving factor for the subsequent CCL1 upregulation, which prompted the migration of small intestinal memory γδT17 cells to the lung. S-Ketamine (S-KT) treatment demonstrated a notable capacity to alleviate acute lung injury through dampening pulmonary Wnt/β-catenin signaling-mediated migration of small intestinal γδT17 cells to the lung. Our findings highlight the significant contribution of the direct migration of immune cells from the small intestine to the lung in sepsis-induced acute lung injury, and clrify the pathological significance of the localized elevation of IL-17A in the lung.

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