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Vagal neuroimmune axis modulates heart failure by limiting monocyte-derived inflammatory CCRL2 macrophage [2]

ABSTRACT: Vagal neuroimmune axis modulates heart failure by limiting monocyte-derived inflammatory CCRL2 macrophage [2]

PROVIDER: PRJNA1256424 | ENA |

REPOSITORIES: ENA

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Vagal neuroimmune axis modulates heart failure by limiting monocyte-derived inflammatory CCRL2 macrophage

Project description:Autonomic neuronal dysfunction is associated with heart failure (HF). Here, we report that targeted vagal nerve stimulation (VNS) using optogenetics attenuates cardiac remodelling and HF induced by pressure overload. Unbiased approaches revealed that VNS decreased the proportion of the Ccrl2+ macrophage subset, which derived from myeloid monocytes and exhibited a distinct tumour necrosis factor-alpha (TNFα)-responsive, pro-hypertrophic, and profibrotic signature. Elimination of Ccrl2+ macrophages prevented cardiac remodelling and HF. Functional characterisation by Ccrl2+ macrophage-specific overexpression or global genetic loss of α7 nicotinic acetylcholine receptor (α7nAChR) highlighted its crucial contribution to VNS-mediated cardioprotection. Mechanistically, activation of α7nAChR inhibited the TNFα responsiveness through upregulated expression of the transcription factor NRF2. Cardiac Ccrl2+ macrophages and TNFα-responsive proteins were positively correlated with cardiac remodelling and dysfunction in humans. Finally, an α7nAChR agonist effectively blocked the development of HF. These results suggest that the vagal neuroimmune axis modulates heart failure and is a promising target for treatment.

2025-05-03 | GSE295812 | GEO

Vagal neuroimmune axis modulates heart failure by limiting monocyte-derived inflammatory CCRL2 macrophage

2025-05-31 | GSE296034 | GEO

Vagal neuroimmune axis modulates heart failure by limiting monocyte-derived inflammatory CCRL2 macrophage [2]

2025-05-03 | GSE295813 | GEO

Vagal neuroimmune axis modulates heart failure by limiting monocyte-derived inflammatory CCRL2 macrophage II

2025-05-31 | GSE296255 | GEO

Vagal neuroimmune axis modulates heart failure by limiting monocyte-derived inflammatory CCRL2 macrophage

Project description:Vagal neuroimmune axis modulates heart failure by limiting monocyte-derived inflammatory CCRL2 macrophage

| PRJNA1256425 | ENA

Vagal neuroimmune axis modulates heart failure by limiting monocyte-derived inflammatory CCRL2 macrophage

Project description:Vagal neuroimmune axis modulates heart failure by limiting monocyte-derived inflammatory CCRL2 macrophage

| PRJNA1257340 | ENA

Vagal neuroimmune axis modulates heart failure by limiting monocyte-derived inflammatory CCRL2 macrophage II

Project description:Vagal neuroimmune axis modulates heart failure by limiting monocyte-derived inflammatory CCRL2 macrophage II

| PRJNA1258276 | ENA

Effect of disturbance of vagal- or COX- dependent route of neuroimmune communication on the hypotalamic transcriptome

Project description:This is data from studies on mechanisms compensating for disturbances in the activity of neuronal or humoral neuroimmune communication pathways in the model of intraperitoneal inflammation.

2022-03-24 | GSE199231 | GEO

Effect of disturbance of vagal- or COX- dependent route of neuroimmune communication on the hypotalamic transcriptome

Project description:Effect of disturbance of vagal- or COX- dependent route of neuroimmune communication on the hypotalamic transcriptome

| PRJNA818997 | ENA

CCRL2 expression by specialized lung capillary endothelial cells controls NK cells homing in lung cancer

Project description:Patterns of chemotactic receptors regulate the homing of leukocytes to tissues. Here we report that the CCRL2/chemerin/CMKLR1 axis represent a selective pathway for the homing of NK cells to the lung. CCRL2 is a non-signaling seven-transmembrane domain receptor able to control lung tumor growth. Total or endothelial cell targeted CCRL2 deletion or the deletion of its ligand chemerin were found to promote tumor progression in a KrasG12D/+;p53LoxP lung cancer model. This phenotype was dependent on the reduced recruitment of CD27-CD11b+ mature NK cells. Mining scRNA-seq databases identified CCRL2 expression as the hallmark of general alveolar lung capillary endothelial cells (gCaps). CCRL2 expression is epigenetically regulated in lung endothelium. In vivo administration of low doses of the demethylating agent 5-Aza induced CCRL2 upregulation, increased recruitment of NK cells and lung protection in a tumor model. These results identify CCRL2 as a NK cell lung homing molecule that might be exploited to promote NK cell-mediated lung immune surveillance.

2023-08-04 | GSE212088 | GEO

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