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Adrenal stress response is an essential host response against lethal T cell activation

ABSTRACT: Adrenal stress response is an essential host response against lethal T cell activation

PROVIDER: PRJNA745198 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15090070_1.fastq.gz	Fastqsanger.gz
	SRR15090070_2.fastq.gz	Fastqsanger.gz
	SRR15090071_1.fastq.gz	Fastqsanger.gz
	SRR15090071_2.fastq.gz	Fastqsanger.gz
	SRR15090072_1.fastq.gz	Fastqsanger.gz

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Adrenal stress response is an essential host response against lethal T cell activation

Project description:Cytokine release syndrome (CRS) is a major cause of death in lethal T cell activation and presents a significant barrier for CAR-T immunotherapy or allogenic hematopoietic cell transplantation. We reported here that adrenal stress response, defined by a 5-10-fold increase in induced glucocorticoid (iGC) production, is an essential host response against lethal T cell activation. We identified scavenger receptor BI (SR-BI), a HDL receptor, as a key regulator for iGC production. Using SR-BI null mice as an adrenal stress response deficiency model, we demonstrated that adrenal stress response protects anti-CD3 induced death through keeping CRS under control and relative adrenal insufficiency (RAI) – lacking adrenal stress response, is a risk factor.

2023-04-19 | GSE179837 | GEO

The adrenal stress response is an essential host response against therapy-induced lethal immune activation.

Project description:Cytokine release syndrome (CRS) is a systemic inflammatory syndrome associated with infection- or drug-induced T cell activation and can cause multiple organ failure and even death. Because current treatments are ineffective in some patients with severe CRS, we set out to identify risk factors and mechanisms behind severe CRS that might lead to preventive therapies and better clinical outcomes in patients. In mice, we found that deficiency in the adrenal stress response-with similarities to such in patients called relative adrenal insufficiency (RAI)-conferred a high risk for lethal CRS. Mice treated with CD3 antibodies were protected against lethal CRS by the production of glucocorticoids (GC) induced by the adrenal stress response in a manner dependent on the scavenger receptor B1 (SR-BI), a receptor for high-density lipoprotein (HDL). Mice with whole-body or adrenal gland-specific SR-BI deficiency exhibited impaired GC production, more severe CRS, and increased mortality in response to CD3 antibodies. Pretreatment with a low dose of GC effectively suppressed the development of CRS and rescued survival in SR-BI-deficient mice without compromising T cell function through apoptosis. Our findings suggest that RAI may be a risk factor for therapy-induced CRS and that pretreating RAI patients with GC may prevent lethal CRS.

| S-EPMC10091512 | biostudies-literature

HIF1α is an essential regulator of steroidogenesis in the adrenal gland

Project description:HIF1α is an essential regulator of steroidogenesis in the adrenal gland

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Epigenetic silencing of interleukin-10 by host-derived oxidized phospholipids supports a lethal inflammatory response to infections supports a lethal inflammatory response to infections

Project description:Epigenetic silencing of interleukin-10 by host-derived oxidized phospholipids supports a lethal inflammatory response to infections supports a lethal inflammatory response to infections

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Epigenetic silencing of interleukin-10 by host-derived oxidized phospholipids supports a lethal inflammatory response to infections supports a lethal inflammatory response to infections

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Expression data from porcine adrenal gland

Project description:To gain insight into the adrenal stress response, we analyzed differential mRNA expression of genes associated with stress induced by aggressive behaviour in the pig In an animal experiment various levels of aggressive behaviour and stress were induced by mixing groups of unfamiliar pigs with different aggressiveness. To analyze adrenal stress response we selected two experimental groups for comparison, each comprising eight animals (n=16) which differed significantly in aggressive behaviour and plasma cortisol levels. To identify differentially expressed genes, we compared the adrenal transcriptome of these two groups of pigs, using the Affymetrix GeneChip porcine Genome Array.

2011-05-31 | E-GEOD-25138 | biostudies-arrayexpress

Genome wide analysis of Adrenal Gland tissue from Gata6 conditional knockout versus Control Adrenal tissue

Project description:Transcription factor GATA6 is expressed in the fetal and adult adrenal cortex and has been implicated in steroidogenesis. To characterize the role of GATA6 in adrenocortical development and function, we generated mice in which Gata6 was conditionally deleted using Cre-LoxP recombination with Sf1-cre. The adrenal glands of adult Gata6 conditional knockout (cKO) mice were small and had a thin cortex with thickened capsule. Cytomegalic changes were evident in the adrenal glands of fetal and adult cKO mice, and chromaffin cells were ectopically located at the periphery of the glands. The secretion of corticosterone in response to exogenous ACTH was blunted in cKO mice. Cells expressing gonadal-like markers, including Gata4, Amhr2, and Tcf21, accumulated in the adrenal capsule and subcapsule of cKO mice, suggesting aberrant adrenocortical progenitor/stem cell differentiation. Gonadectomy triggered the overexpression of sex steroidogenic differentiation markers, such as Lhcgr and Cyp17, in the adrenal glands of male and female cKO mice. Nulliparous female and orchiectomized male cKO mice lacked an adrenal X-zone. Microarray hybridization identified Pik3c2g as a novel X-zone marker that is downregulated in the adrenal glands of nulliparous female Gata6 cKO mice. Our findings offer genetic proof of the longstanding hypothesis that GATA6 regulates the differentiation of steroidogenic progenitors into corticoid-producing cells. 3 replicates from both conditional knockout of Gata6 in the adrenal gland and control adrenal glands from non-knockout mice were compared

2013-06-06 | E-GEOD-40398 | biostudies-arrayexpress

Decoding the human adrenal cortex matrisome: the composition and regulation of ECM proteins of the outer and inner microenvironment.

Project description:The extracellular matrix (ECM) comprises macromolecules that shape a complex three-dimensional network. Filling the intercellular space and playing a crucial role in the structure and function of tissues, ECM regulates essential cellular processes such as adhesion, differentiation, and cell signaling. In the human adrenal gland, composed of cortex and medulla surrounded by a capsule, the ECM has not yet been directly described, although its impact on the processes of proliferation and steroidogenesis of the adrenal cortex is recognized. This study proposes a comprehensive analysis aims to comprehensively analyze the ECM of the adult human adrenal cortex, which is separated into outer fraction (OF) and inner fraction (IF), by comparing their proteomic profiles. The study discusses the composition, spatial distribution, and relevance of differentially expressed ECM signatures of the adrenal cortex matrisome on adrenal structure and function. The findings were validated through database analysis (cross-validation), histochemical, and immunohistochemical approaches. A total of 121 ECM proteins were identified and categorized into glycoproteins, collagens, ECM regulators, proteoglycans, ECM-affiliated proteins, and secreted factors. Thirty-one ECM proteins were identified only in OF, 9 only in IF, and 81 were identified in common with both fractions. Additionally, 106 ECM proteins were cross-validated using Human matrisome DB 2.0 and the proteins differentially expressed in OF and IF, were identified. This study provides significant insights into the composition and regulation of the ECM in the human adrenal cortex, shedding light on the adrenal microenvironment and its role in the functioning, maintenance, and renewal of the adrenal gland.

2024-09-11 | PXD051801 | Pride

Transcriptomic analysis of Helicobacter pylori 26695 exposed to lethal concentration of a bactericidal inhibitor of the essential response regulator HsrA

Project description:Transcriptomic analysis of Helicobacter pylori 26695 exposed to lethal concentration of a bactericidal inhibitor of the essential response regulator HsrA

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Transcriptomic analysis of Helicobacter pylori 26695 exposed to lethal concentration of a bactericidal inhibitor of the essential response regulator HsrA

Project description:Helicobacter pylori, a pathogenic member of phylum Campylobacterota (formerly Epsilonproteobacteria), is recognized as the leading cause of several human gastric pathologies, including acute and chronic gastritis, peptic ulcer disease, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. In the last two decades, the alarming increase of the antibiotic resistance levels to first-line and even “rescue” antibiotics, especially clarithromycin, metronidazole and levofloxacin, has led to a marked decrease of the eradication rates of traditional therapies. In previous works, we have validated the essential protein HsrA as an effective therapeutic target for H. pylori infection. HsrA is an OmpR/PhoB-type orphan response regulator, unique and highly conserved in members of phylum Campylobacterota, which appears involved in a variety of crucial physiological processes. In the present work, we carried out a transcriptomic analysis in order to discern the global effects of lethal concentrations of a bactericidal HsrA inhibitor on the H. pylori physiology. Treatment with the bactericidal HsrA inhibitor significantly changed the transcript levels of 367 open reading frames (ORF), of which 212 genes appeared upregulated and 155 genes resulted in downregulation, as compared with control samples. Thus, in vivo HsrA inhibition influenced, directly or indirectly, the expression of 23% of ORFs encoded by the H. pylori 26696 genome. Among the 268 differentially expressed genes (DEGs) with defined functions, two functional categories were highly enriched with downregulated genes involved in essential physiological processes: (1) ribosome biogenesis, and (2) electron transfer and oxidative phosphorylation.

2024-09-21 | E-MTAB-14255 | biostudies-arrayexpress

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