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Hypothalamus response to LPS and restraint stress

ABSTRACT: The paraventricular hypothalamic nucleus (PVH) is a key site for integrating neuroendocrine, autonomic, and behavioral adjustments to diverse homeostatic challenges, including "physiological" (e.g., infection or hemorrhage) and "emotional" [e.g., restraint (RST) or footshock] stresses. Both types of challenges ultimately converge to activate common response systems represented in PVH, including the hypothalamo-pituitary-adrenal axis and the sympathoadrenal system. Oligonucleotide microarrays (U74A; Affymetrix, Santa Clara, CA) were used to compare and contrast gene expression profiles in the PVH elicited at 1 and 3 hr after acute exposure to representative physiological [intraperitoneal injection of 10 microg lipopolysaccharide (LPS)] and emotional (30 min RST) stressors. In general, the two challenges recruited relatively few genes in common, with the degree of overlap varying across functional classes of genes. The greatest degree of commonality was seen among signaling molecules and neuropeptides, whereas transcription factors upregulated by RST and LPS were largely distinct. Unexpectedly, RST induced a number of immune-related molecules, which were not regulated by LPS. Hybridization histochemical analyses localized a subset of responsive transcripts to the PVH and/or immediately adjoining regions. Immunerelated molecules in particular distributed broadly to vascular and other barrier-associated cell types. These global transcriptional profiles inform the search for early (transcription factors) and late (target genes) mechanisms in the modulation of PVH, and generalized CNS, responses to categorically distinct stressors. Keywords: other

ORGANISM(S): Mus musculus

PROVIDER: GSE367 | GEO | 2003/04/17

SECONDARY ACCESSION(S): PRJNA84867

REPOSITORIES: GEO

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Transcription profiling of paraventricular hypothalamic nucleus (PVH) from mice stimulated by either LPS injection or restraint to understand the molecular mechanisms in the modulation of PVH responses to categorically distinct stressors.

Project description:The paraventricular hypothalamic nucleus (PVH) is a key site for integrating neuroendocrine, autonomic, and behavioral adjustments to diverse homeostatic challenges, including physiological (e.g., infection or hemorrhage) and emotional [e.g., restraint (RST) or footshock] stresses. Both types of challenges ultimately converge to activate common response systems represented in PVH, including the hypothalamo-pituitary-adrenal axis and the sympathoadrenal system. Oligonucleotide microarrays (U74A; Affymetrix, Santa Clara, CA) were used to compare and contrast gene expression profiles in the PVH elicited at 1 and 3 hr after acute exposure to representative physiological [intraperitoneal injection of 10 microg lipopolysaccharide (LPS)] and emotional (30 min RST) stressors. In general, the two challenges recruited relatively few genes in common, with the degree of overlap varying across functional classes of genes. The greatest degree of commonality was seen among signaling molecules and neuropeptides, whereas transcription factors upregulated by RST and LPS were largely distinct. Unexpectedly, RST induced a number of immune-related molecules, which were not regulated by LPS. Hybridization histochemical analyses localized a subset of responsive transcripts to the PVH and/or immediately adjoining regions. Immunerelated molecules in particular distributed broadly to vascular and other barrier-associated cell types. These global transcriptional profiles inform the search for early (transcription factors) and late (target genes) mechanisms in the modulation of PVH, and generalized CNS, responses to categorically distinct stressors.

2007-11-01 | E-GEOD-367 | biostudies-arrayexpress

Chronic Restraint Stress Upregulates Erythropoiesis Through Glucocorticoid Stimulation

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2016-06-07 | GSE47725 | GEO

Different DNA methylation between hypothalamus paraventricular (PVH) and ventromedial (VMH) nuclei

Project description:The goal is to compare the DNA methylation patterns between ARH and PVH to examine to what extent DNA methylation is region specific in genome scale. ARH and PVH were micro-dissected from mice brains. Each 7 pieces of ARH or PVH were pooled and used for DNA methylation comparison by methylation specific amplification microarray (MSAM). As a brief description of the MSAM: 500ng of genomic DNA was serially digested with SmaI and XmaI followed by an adaptor ligation and adaptor mediated PCR amplification and then cohybridization. Two-color cohybridizations were performed as paired comparison of PVH vs. ARH with two biological replicates including dye swap.

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LPS tolerance in macrophages

Project description:Among the multiple mechanisms that control the intensity and duration of macrophage activation, the development of a state of refractoriness to a second stimulation in cells treated with LPS has long been recognized. Release of inhibitory cytokines and alterations in intracellular signaling pathways may be involved in the development of LPS tolerance. Although a number of molecules have been implicated, a detailed picture of the molecular changes in LPS tolerance is still missing. We have used a genome-wide gene expression analysis approach to (i) define which fraction of LPS target genes are subject to tolerance induction and (ii) identify genes that are expressed at high levels in tolerant macrophages. Our data show that in LPS tolerant macrophages the vast majority of LPS-induced gene expression is abrogated. The extent of tolerance induction varies for individual genes, and a small subset appears to be excepted. Compared to other negative control mechanisms of macrophages, e.g. IL-10-induced deactivation, LPS-tolerance inhibits a much wider range of transcriptional targets. Some previously described negative regulators of TLR-signaling (e.g. IRAK-M) were confirmed as expressed at higher levels in LPS-tolerant macrophages. In addition, we discuss other potential players in LPS tolerance identified in this group of genes. Keywords: pre and restimulation with LPS, tolerance induction

2007-08-10 | GSE8621 | GEO

Transcription profiling of mouse macrophages exposed to LPS

Project description:Among the multiple mechanisms that control the intensity and duration of macrophage activation, the development of a state of refractoriness to a second stimulation in cells treated with LPS has long been recognized. Release of inhibitory cytokines and alterations in intracellular signaling pathways may be involved in the development of LPS tolerance. Although a number of molecules have been implicated, a detailed picture of the molecular changes in LPS tolerance is still missing. We have used a genome-wide gene expression analysis approach to (i) define which fraction of LPS target genes are subject to tolerance induction and (ii) identify genes that are expressed at high levels in tolerant macrophages. Our data show that in LPS tolerant macrophages the vast majority of LPS-induced gene expression is abrogated. The extent of tolerance induction varies for individual genes, and a small subset appears to be excepted. Compared to other negative control mechanisms of macrophages, e.g. IL-10-induced deactivation, LPS-tolerance inhibits a much wider range of transcriptional targets. Some previously described negative regulators of TLR-signaling (e.g. IRAK-M) were confirmed as expressed at higher levels in LPS-tolerant macrophages. In addition, we discuss other potential players in LPS tolerance identified in this group of genes. Experiment Overall Design: Cells were either prestimulated (1_X) or not (0_X) for 18h with 100 ng/ml LPS. Media was exchanged and after 2h rest, cells either restimulated (X_1) or not (X_0) with again 100 ng/ml LPS. This resulted in 4 experimental conditions: 0_0, 0_1, 1_0 and 1_1. There were 3 biological replicates done, resulting in 12 arrays altogether.

2008-06-16 | E-GEOD-8621 | biostudies-arrayexpress

Small molecule screening identifies Syk kinase inhibition and Rutaecarpine as modulators of macrophage training and SARS CoV-2 infection

Project description:Biologically active small molecules can impart modulatory effects in immune cells, in some cases, providing extended long-term memory. In a screen of biologically active small molecules for regulators of TNF induction, we identified several compounds with the ability to induce training effects on human macrophages. Rutaecarpine was identified both as an acute and long-term modulator, enhancing LPS-induced pro-inflammatory cytokine secretion and relieving LPS tolerance in human macrophages. Rutaecarpine inhibited β-glucan-induced H3K4Me3 marks at the promoters of several proinflammatory cytokines, highlighting the potential of this molecule to modulate 47 epigenetic topology. In further work, a Syk kinase inhibitor (SYKi IV) screen hit promoted an enhanced response to LPS similar to that previously reported for β-glucan-induced training. Macrophages trained with SYKi IV showed a high degree of resistance to influenza A, multiple variants of SARS CoV-2 and OC43 coronavirus infection, highlighting a potential application of this molecule and other Syk kinase inhibitors as a prophylactic treatment for viral susceptibility.

2022-09-26 | GSE210476 | GEO

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Unique Genetic Responses Revealed in RNA-seq of the Spleen of Chickens Stimulated with Lipopolysaccharide and Heat

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The landscape of abiotic and biotic stress-responsive splice variants with deep RNA-seq datasets in hot pepper

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