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The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells [F1413]

ABSTRACT: The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells [F1413]

PROVIDER: PRJNA673314 | ENA |

REPOSITORIES: ENA

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	SRR12931603.fastq.gz	Fastqsanger.gz
	SRR12931604.fastq.gz	Fastqsanger.gz

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The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells [F1347]

Project description:Extracellular adenosine triphosphate (ATP) released by mucosal immune cells and by microbiota in the intestinal lumen elicits diverse immune responses that mediate the intestinal homeostasis via P2 purinergic receptors, while overactivation of the ATP signaling leads to disruption of mucosal immune system linked to pathogenesis of intestinal inflammation. In the small intestine, hydrolysis of luminal ATP by E-NTPD7 in epithelial cells is essential for control of the number of Th17 cells. However, the molecular mechanism underlying regulation of microbiota-derived ATP in the colon is poorly understood. Here, we show that E-NTPD8 is highly expressed in large intestinal epithelial cells and hydrolyzes microbiota-derived luminal ATP. Compared to wild-type mice, Entpd8-/- mice develop more severe DSS-induced colitis. In this context, either depletion of neutrophils and monocytes by injecting with anti-Gr-1 antibody or introduction of P2rx4 deficiency into hematopoietic cells ameliorates colitis in Entpd8-/- mice. Increased level of luminal ATP in the colon of Entpd8-/- mice promotes glycolysis in neutrophils and monocytes through P2X4 receptor-dependent Ca2+ influx, which links to prolonged survival and elevated ROS production in these cells. Together, these results indicate that E-NTPD8 limits intestinal inflammation by controlling metabolic alteration toward glycolysis via P2X4 receptor in myeloid cells.

2021-09-23 | GSE160380 | GEO

The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells [F0536]

2021-09-23 | GSE160379 | GEO

The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells [F1413]

2021-09-23 | GSE160381 | GEO

The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells

Project description:The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells

| PRJNA673145 | ENA

The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells [F0536]

Project description:The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells [F0536]

| PRJNA673313 | ENA

The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells [F1347]

Project description:The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells [F1347]

| PRJNA673312 | ENA

The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colonic inflammation through regulation of P2X4 receptor-dependent metabolism in myeloid cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-09-23 | GSE160382 | GEO

The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colitis through modulation of P2X4 receptor-dependent metabolism in myeloid cells.

Project description: Not available

| S-EPMC8488689 | biostudies-literature

P2X4 Drives Sex-Specific Neuroprotection in Autoimmune Neuroinflammation

Project description:Microglia critically influence multiple sclerosis (MS) pathophysiology through debris clearance, myelin repair, and modulation of neuroinflammation. These processes are partly regulated by ATP-gated ion channel P2X4, predominantly expressed in microglia. We previously reported that ivermectin (IVM), a positive allosteric modulator of P2X4, promotes myelin phagocytosis, remyelination, and functional recovery in experimental autoimmune encephalomyelitis (EAE). Here, we dissected the cellular basis of P2X4-mediated effects using P2X4mCherryIN knock-in (P2X4KI) mice, in which P2X4 is replaced by a non-internalized variant (P2X4KI), leading to increased surface localization at the plasma membrane. Constitutive and myeloid-specific P2X4KI (Cd11b-P2X4KI) mice showed significant amelioration of EAE motor deficits, although exclusively in females. Despite equivalent P2X4 expression, function, and IVM responsiveness between sexes, progesterone potentiated P2X4 currents and prolonged channel deactivation, revealing direct hormonal modulation of P2X4 gating. Notably, ovariectomy abolished P2X4-mediated protection in females, confirming the requirement of female hormones. These findings identify microglial P2X4 as a critical modulator of neuroinflammatory outcomes and uncover a previously unrecognized hormone–P2X4 interaction that underlies sex-specific disease modulation. Targeting this pathway may enable precision therapies for MS.

2026-03-14 | GSE324320 | GEO

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Project description:Sepsis causes millions of deaths per year worldwide and is a current global health priority declared by the WHO. Sepsis-related deaths are a result of dysregulated inflammatory immune responses indicating the need to develop strategies to target inflammation. An important mediator of inflammation is extracellular adenosine triphosphate (ATP) that is secreted by inflamed host cells and tissues, and also by bacteria in a strain-specific and growth phase-dependent manner. Here, we investigated the mechanisms by which bacteria release ATP. Using genetic mutant strains of Escherichia coli (E. coli), we demonstrate that ATP release is dependent on ATP synthase within the inner bacterial membrane. In addition, impaired integrity of the outer bacterial membrane and bacterial death notably contribute to ATP release. In a mouse model of abdominal sepsis, local effects of bacterial ATP were analysed using a transformed E. coli bearing an arabinose-inducible periplasmic apyrase hydrolyzing ATP to be released. Abrogating bacterial ATP release shows that bacterial ATP suppresses local immune responses, resulting in reduced neutrophil counts and impaired survival. In addition, bacterial ATP has systemic effects via its transport in outer membrane vesicles (OMV). ATP-loaded OMV are quickly distributed throughout the body and upregulated expression of genes activating degranulation in neutrophils, potentially contributing to the exacerbation of sepsis severity. This study reveals mechanisms of bacterial ATP release and its local and systemic roles in sepsis pathogenesis.

2024-07-16 | GSE272296 | GEO

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