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IMPACT OF INTERLEUKIN 10 DEFICIENCY ON INTESTINAL EPITHELIUM RESPONSES TO INFLAMMATORY SIGNALS

ABSTRACT: IMPACT OF INTERLEUKIN 10 DEFICIENCY ON INTESTINAL EPITHELIUM RESPONSES TO INFLAMMATORY SIGNALS

PROVIDER: PRJEB44033 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR5630260_1.fastq.gz	Fastqsanger.gz
	ERR5630260_2.fastq.gz	Fastqsanger.gz
	ERR5630270_1.fastq.gz	Fastqsanger.gz
	ERR5630270_2.fastq.gz	Fastqsanger.gz
	ERR5630261_1.fastq.gz	Fastqsanger.gz

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IMPACT OF INTERLEUKIN 10 DEFICIENCY ON INTESTINAL EPITHELIUM RESPONSES TO INFLAMMATORY SIGNALS

Project description:Interleukin-10 (IL-10) is a pleiotropic, anti-inflammatory cytokine that has a major protective role in the intestine. Although its production by cells of the innate and adaptive immune system have been extensively studied, its intrinsic role in intestinal epithelial cells is poorly understood. In this study, we utilised ATAC and RNA sequencing to define the transcriptional response of murine enteroids to tumour necrosis factor (TNF). We identified that the key early phase drivers of the transcriptional response within intestinal epithelium wereNFkB transcription factor dependent. TNF-induced Il10-/- enteroids showed significant downregulation of identified NFkB target genes Tnf and Ccl20, and delayed overexpression of genes encoding NFkB inhibitors, Nfkbia and Tnfaip3. Similar responses were observed in vivo. IL-10 deficiency also impacted on TNF-induced endogenous NFkB activation. Intestinal epithelium-derived IL-10 appears to play a crucial autocrine role in regulating NFkB-dependent transcriptional response to an inflammatory environment and a potential target for therapeutic intervention.

2021-12-30 | E-MTAB-10217 | biostudies-arrayexpress

Impact of Interleukin 10 Deficiency on Intestinal Epithelium Responses to Inflammatory Signals.

Project description:Interleukin 10 (IL-10) is a pleiotropic, anti-inflammatory cytokine that has a major protective role in the intestine. Although its production by cells of the innate and adaptive immune system has been extensively studied, its intrinsic role in intestinal epithelial cells is poorly understood. In this study, we utilised both ATAC sequencing and RNA sequencing to define the transcriptional response of murine enteroids to tumour necrosis factor (TNF). We identified that the key early phase drivers of the transcriptional response to TNF within intestinal epithelium were NFκB transcription factor dependent. Using wild-type and Il10-/- enteroid cultures, we showed an intrinsic, intestinal epithelium specific effect of IL-10 deficiency on TNF-induced gene transcription, with significant downregulation of identified NFκB target genes Tnf, Ccl20, and Cxcl10, and delayed overexpression of NFκB inhibitor encoding genes, Nfkbia and Tnfaip3. IL-10 deficiency, or immunoblockade of IL-10 receptor, impacted on TNF-induced endogenous NFκB activity and downstream NFκB target gene transcription. Intestinal epithelium-derived IL-10 appears to play a crucial role as a positive regulator of the canonical NFκB pathway, contributing to maintenance of intestinal homeostasis. This is particularly important in the context of an inflammatory environment and highlights the potential for future tissue-targeted IL-10 therapeutic intervention.

| S-EPMC8244292 | biostudies-literature

Interleukin-17 governs hypoxic adaptation of injured epithelium

Project description:Interleukin-17 governs hypoxic adaptation of injured epithelium

| PRJNA702447 | ENA

Macrophage-restricted Interleukin-10 receptor-, but not IL-10 deficiency causes severe spontaneous colitis

Project description:Interleukin-10 (IL-10) is a pleiotropic anti-inflammatory cytokine produced and sensed by most hematopoietic cells. Genome wide association studies and experimental animal models point at a central role of the IL-10 axis in Inflammatory Bowel Diseases. Here we investigated the importance of intestinal macrophage production of IL-10 and their IL-10 exposure, as well as the existence of an IL-10-based autocrine regulatory loop in the gut. Specifically, we generated mice harboring IL-10 or IL-10 receptor (IL-10R?) mutations in intestinal lamina propria-resident chemokine receptor CX3CR1hi-expressingmacrophages. We found macrophage-derived IL-10 dispensable for gut homeostasis and maintenance of colonic T regulatory cells. In contrast, loss of IL-10 receptor expression impaired the critical conditioning of these monocyte-derived macrophages, but resulted in spontaneous development of severe colitis. Collectively, our results highlight IL-10 as a critical homeostatic macrophage-conditioning factor in the colon and define intestinal CX3CR1hi macrophages as a decisive factor that determines gut health or inflammation. Microarray of resident macrophages sorted from colons of Interleukin-10 deficeint mice and macrophage-restricted interleukin-10 receptor deficient mice versus colonic resident macrophages of wild type mice

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Interleukin-17 governs hypoxic adaptation of injured epithelium [spatial transcriptomics]

Project description:Interleukin-17 governs hypoxic adaptation of injured epithelium [spatial transcriptomics]

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Interleukin-17 governs hypoxic adaptation of injured epithelium [bulk RNA-seq]

Project description:Interleukin-17 governs hypoxic adaptation of injured epithelium [bulk RNA-seq]

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Macrophage-restricted Interleukin-10 receptor-, but not IL-10 deficiency causes severe spontaneous colitis

Project description:Interleukin-10 (IL-10) is a pleiotropic anti-inflammatory cytokine produced and sensed by most hematopoietic cells. Genome wide association studies and experimental animal models point at a central role of the IL-10 axis in Inflammatory Bowel Diseases. Here we investigated the importance of intestinal macrophage production of IL-10 and their IL-10 exposure, as well as the existence of an IL-10-based autocrine regulatory loop in the gut. Specifically, we generated mice harboring IL-10 or IL-10 receptor (IL-10Rα) mutations in intestinal lamina propria-resident chemokine receptor CX3CR1hi-expressingmacrophages. We found macrophage-derived IL-10 dispensable for gut homeostasis and maintenance of colonic T regulatory cells. In contrast, loss of IL-10 receptor expression impaired the critical conditioning of these monocyte-derived macrophages, but resulted in spontaneous development of severe colitis. Collectively, our results highlight IL-10 as a critical homeostatic macrophage-conditioning factor in the colon and define intestinal CX3CR1hi macrophages as a decisive factor that determines gut health or inflammation.

2014-05-09 | GSE56444 | GEO

Interleukin-17-Mediated Protective Cytokine Signaling Against Degeneration of the Retinal Pigment Epithelium

Project description:Interleukin-17-Mediated Protective Cytokine Signaling Against Degeneration of the Retinal Pigment Epithelium

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Interleukin-17-Mediated Protective Cytokine Signaling Against Degeneration of the Retinal Pigment Epithelium

Project description:Injuries to the retinal pigment epithelium (RPE) and outer retina often result in the accumulation of retinal microglia within the subretinal space. These subretinal microglia play crucial roles in inflammation and resolution, but the mechanisms governing their functions are still largely unknown. Our previous research highlighted the protective functions of choroidal gd T cells in response to RPE injury. In the current study, we employed single-cell RNA sequencing approach to delve deeper into the mechanisms involved. We found that gd T cells were the primary producer of interleukin-17 (IL-17) in the choroid. IL-17 signaled through its receptor on the RPE, subsequently triggering the production of interleukin-6 (IL-6). This cascade of cytokines initiated a metabolic reprogramming of subretinal microglia, enhancing their capacity for lipid metabolism. RPE-specific knockout of IL-17 receptor A led to the dysfunction of subretinal microglia and RPE pathology. Collectively, our findings suggest that responding to RPE injury, the choroidal gd T cells can initiate a protective signaling cascade that ensures the proper functioning of subretinal microglia.

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Maladaptive TGF-β Signals to the Alveolar Epithelium Drive Fibrosis after COVID-19 Infection

Project description:Maladaptive TGF-β Signals to the Alveolar Epithelium Drive Fibrosis after COVID-19 Infection

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