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A type 1 immune-stromal cell network mediates disease tolerance and barrier protection against intestinal infection

ABSTRACT: A type 1 immune-stromal cell network mediates disease tolerance and barrier protection against intestinal infection

PROVIDER: PRJNA1238905 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32796517_1.fastq.gz	Fastqsanger.gz
	SRR32796517_2.fastq.gz	Fastqsanger.gz
	SRR32796518_1.fastq.gz	Fastqsanger.gz
	SRR32796518_2.fastq.gz	Fastqsanger.gz
	SRR32796519_1.fastq.gz	Fastqsanger.gz

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A type 1 immune-stromal cell network mediates disease tolerance and barrier protection against intestinal infection

Project description:Type 1 immunity mediates host defense through pathogen elimination, but whether this pathway also impacts tissue function is unknown. Here we demonstrate that rapid induction of IFNγ signaling coordinates a multi-cellular response that is critical to limit tissue damage and maintain gut motility following infection of mice with a tissue-invasive helminth. IFNγ production is initiated by antigen-independent activation of lamina propria CD8+ T cells following MyD88-dependent recognition of the microbiota during helminth-induced barrier invasion. IFNγ acted directly on intestinal stromal cells to recruit neutrophils that limited parasite-induced tissue injury. IFNγ sensing also limited the expansion of smooth muscle actin-expressing cells to prevent pathological gut dysmotility. Importantly, this tissue-protective response had limited impact on parasite burden, indicating that IFNγ supports a disease tolerance defense strategy. Our results have important implications for managing the pathophysiological sequelae of post-infectious gut dysfunction and chronic inflammatory diseases associated with stromal remodelling.

2025-03-25 | GSE292516 | GEO

Stromal protection against low dose AraC induced differentiation in U937 cells

Project description:Stromal protection against low dose AraC induced differentiation in U937 cells

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Stromal protection against low dose AraC induced differentiation in U937 cells

Project description:Low dose AraC (LDAC) is a commonly used treatment approach in AML patients unfit for standard chemotherapy. However the mechanism of action is still not completely elucidated. Induction of differentiation after LDAC has been described in vitro, but is rarely seen in vivo. We have demonstrated the protective action of stromal cells in LDAC-mediated induction of differentiation. here we enclose the changes in gene expression in U937 cells treated with low and high dose AraC with or without stromal support.

2023-11-01 | E-MTAB-13192 | biostudies-arrayexpress

Anthocyanin protection against PCBs

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LPS-induced systemic inflammation mediates a protective effect against ischemic injury via microglia

Project description:LPS-induced systemic inflammation mediates a protective action on ischemic injury via microglia. We used RNA sequencing analysis (RNA-seq) to gain molecular insights into microglia-mediated protection of cerebral infarction.

2023-12-19 | GSE244358 | GEO

Tetracycline-induced mitohormesis mediates disease tolerance against influenza

Project description:Tetracycline-induced mitohormesis mediates disease tolerance against influenza

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Cardiac microvascular barrier function mediates the protection of Tongxinluo against myocardial ischemia/reperfusion injury.

Project description:ObjectiveTongxinluo (TXL) has been shown to decrease myocardial necrosis after ischemia/reperfusion (I/R) by simulating ischemia preconditioning (IPC). However, the core mechanism of TXL remains unclear. This study was designed to investigate the key targets of TXL against I/R injury (IRI) among the cardiac structure-function network.Materials and methodsTo evaluate the severity of lethal IRI, a mathematical model was established according to the relationship between myocardial no-reflow size and necrosis size. A total of 168 mini-swine were employed in myocardial I/R experiment. IRI severity among different interventions was compared and IPC and CCB groups were identified as the mildest and severest groups, respectively. Principal component analysis was applied to further determine 9 key targets of IPC in cardioprotection. Then, the key targets of TXL in cardioprotection were confirmed.ResultsNecrosis size and no-reflow size fit well with the Sigmoid Emax model. Necrosis reduction space (NRS) positively correlates with I/R injury severity and necrosis size (R2=0.92, R2=0.57, P<0.01, respectively). Functional and structural indices correlate positively with NRS (R2=0.64, R2=0.62, P<0.01, respectively). TXL recovers SUR2, iNOS activity, eNOS activity, VE-cadherin, β-catenin, γ-catenin and P-selectin with a trend toward the sham group. Moreover, TXL increases PKA activity and eNOS expression with a trend away from the sham group. Among the above nine indices, eNOS activity, eNOS, VE-cadherin, β-catenin and γ-catenin expression were significantly up-regulated by TXL compared with IPC (P>0.05) or CCB (P<0.05) and these five microvascular barrier-related indices may be the key targets of TXL in minimizing IRI.ConclusionsOur study underlines the lethal IRI as one of the causes of myocardial necrosis. Pretreatment with TXL ameliorates myocardial IRI through promoting cardiac microvascular endothelial barrier function by simulating IPC.

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COX-2 mediates tumor-stromal Prolactin signaling to initiate tumorigenesis

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Serine and 1-carbon metabolism are required for HIF-mediated protection against retinopathy of prematurity

Project description:We determined which metabolic pathways are activated by hypoxia-inducible factor 1-mediated (HIF-1-mediated) protection against oxygen-induced retinopathy (OIR) in newborn mice, the experimental correlate to retinopathy of prematurity, a leading cause of infant blindness. HIF-1 coordinates the change from oxidative to glycolytic metabolism and mediates flux through serine and 1-carbon metabolism (1CM) in hypoxic and cancer cells. We used untargeted metabolite profiling in vivo to demonstrate that hypoxia mimesis activates serine/1CM. Both [13C6] glucose labeling of metabolites in ex vivo retinal explants as well as in vivo [13C3] serine labeling of metabolites followed in liver lysates strongly suggest that retinal serine is primarily derived from hepatic glycolytic carbon and not from retinal glycolytic carbon in newborn pups. In HIF-1α2lox/2lox albumin-Cre-knockout mice, reduced or near-0 levels of serine/glycine further demonstrate the hepatic origin of retinal serine. Furthermore, inhibition of 1CM by methotrexate blocked HIF-mediated protection against OIR. This demonstrated that 1CM participates in protection induced by HIF-1 stabilization. The urea cycle also dominated pathway enrichment analyses of plasma samples. The dependence of retinal serine on hepatic HIF-1 and the upregulation of the urea cycle emphasize the importance of the liver to remote protection of the retina.

2019-07-05 | MTBLS856 | MetaboLights

Trim2b mediates protection against SVCV infection by degrading NLRP12-like and viral SVCV-N/SVCV-G proteins

Project description:Trim2b mediates protection against SVCV infection by degrading NLRP12-like and viral SVCV-N/SVCV-G proteins

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