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Hydroxypropyl-β-cyclodextrin spikes local inflammation that induces Th2 and Tfh responses to the coadministered antigen

ABSTRACT: Gene expression data from mouse organs after hydroxypropyl-β-cyclodextrin injection Cyclodextrins are commonly used as a safe excipient to enhance the solubility and bioavailability of hydrophobic pharmaceutical agents. In this study, we reprofiled hydroxypropyl-β-cyclodextrin (HP-β-CD) as a vaccine adjuvant, and found that it acts as a potent and unique adjuvant.

ORGANISM(S): Mus musculus

PROVIDER: GSE63332 | GEO | 2015/02/15

SECONDARY ACCESSION(S): PRJNA267528

REPOSITORIES: GEO

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Hydroxypropyl-Î²-cyclodextrin spikes local inflammation that induces Th2 and Tfh responses to the coadministered antigen

Project description:Gene expression data from mouse organs after hydroxypropyl-Î²-cyclodextrin injection Cyclodextrins are commonly used as a safe excipient to enhance the solubility and bioavailability of hydrophobic pharmaceutical agents. In this study, we reprofiled hydroxypropyl-Î²-cyclodextrin (HP-Î²-CD) as a vaccine adjuvant, and found that it acts as a potent and unique adjuvant. C57BL/6J mice (6 week old, male, n = 3) were injected i.d. or i.p. with a total volume of 200 micro liter of 30% HP-Î²-CD in PBS. The vehicle-control mice (n = 3) were injected with the same volume of PBS. After 6 h, the inguinal LNs, Liver, and Spleen were removed (within one hour for all samples) and global gene expression was obtained by Affymetrix GeneChip.

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Cyclodextrin treatment leads to atherosclerosis regression by dissolution of cholesterol crystals and LXR activation

Project description:Atherosclerosis is an inflammatory disease linked to elevated blood cholesterol levels. Since cholesterol retention and cholesterol crystals in arterial walls are key pathogenetic factors for atherogenesis, we assessed the therapeutic potential of increasing cholesterol solubility in vivo. Here we show that treatment of murine atherosclerosis with the cyclic oligosaccharide 2-hydroxypropyl-β-cyclodextrin (CD), a compound that solubilizes lipophilic substances, reduced atherosclerotic plaque size, cholesterol crystal (CC) load and promoted plaque regression even under continuing Western diet. CD solubilized CC and promoted cholesterylester and oxysterol production in macrophages leading to liver X receptor-mediated transcriptional reprogramming with increased cholesterol efflux and decreased inflammation. CD treatment may thus be used to increase cholesterol solubility and clearance to prevent or treat atherosclerosis.

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2-hydroxypropyl-beta-cyclodextrin treatment induces modest immune activation in healthy rhesus macaques

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Transcriptome of 2-hydroxypropyl-beta-cyclodextrin treatment in Niemann-Pick disease type C1

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Transcriptome of 2-hydroxypropyl-beta-cyclodextrin treatment in Niemann-Pick disease type C1

Project description:Transcriptome of 2-hydroxypropyl-beta-cyclodextrin treatment in Niemann-Pick disease type C1

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2-hydroxypropyl-beta-cyclodextrin treatment induces modest immune activation in healthy rhesus macaques [ATAC-seq]

Project description:Experimental SIV infection of Asian macaques is an excellent model for HIV disease progression and therapeutic development. Recent coformulations of nucleoside analogs and an integrase inhibitor have been used for parenteral antiretroviral (ARV) administration in SIV-infected macaques, successfully resulting in undetectable plasma SIV RNA. In a cohort of SIVmac239-infected macaques, we recently observed that administration of co-formulated ARVs resulted in an unexpected increase in plasma levels of soluble CD14 (sCD14), associated with stimulation of myeloid cells. We hypothesized that the coformulation solubilizing agentKleptoseTM(2-hydroxypropyl-beta-cyclodextrin; HPβCD) may induce inflammation with myeloid cell activation and the release of sCD14. Herein, we stimulated peripheral blood mononuclear cells (PBMCs) from healthy macaques with HPβCD from different commercial sources and evaluated inflammatory cytokine productionin vitro.Treatment of PBMCs resulted in increased sCD14 release and myeloid cell IL-1bproduction - with stimulation varyingsignificantlyby HPβCD source - and destabilized lymphocyte CCR5 surface expression.We further treated healthy macaques withKleptosealone.In vivo, we observed modestly increased myeloid cell activation in response to Kleptose treatment without significant perturbation of the immunological transcriptome or epigenome.Our resultsdemonstrate a need for vehicle-only controls and highlight immunological perturbations that can occur when using HPβCD in pharmaceutical co-formulations.

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2-hydroxypropyl-beta-cyclodextrin treatment induces modest immune activation in healthy rhesus macaques [RNA-seq]

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2-hydroxypropyl-beta-cyclodextrin treatment induces modest immune activation in healthy rhesus macaques [ATAC-seq]

Project description:2-hydroxypropyl-beta-cyclodextrin treatment induces modest immune activation in healthy rhesus macaques [ATAC-seq]

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2-hydroxypropyl-beta-cyclodextrin treatment induces modest immune activation in healthy rhesus macaques [RNA-seq]

Project description:2-hydroxypropyl-beta-cyclodextrin treatment induces modest immune activation in healthy rhesus macaques [RNA-seq]

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Cyclodextrin promotes atherosclerosis regression via LXR activation (II)

Project description:Atherosclerosis is an inflammatory disease linked to elevated blood cholesterol levels. Despite ongoing advances in the prevention and treatment of atherosclerosis 1, cardiovascular disease remains the leading cause of death worldwide 2. Continuous retention of apolipoprotein B-containing lipoproteins in the subendothelial space causes a local overabundance of free cholesterol. Since cholesterol accumulation and deposition of cholesterol crystals (CCs) triggers a complex inflammatory response 3 4, we tested the therapeutic potential of increasing cholesterol solubility in experimental atherogenesis. Here we show that treatment of murine atherosclerosis with the cyclic oligosaccharide 2-hydroxypropyl-β-cyclodextrin (CD), a compound that solubilizes lipophilic substances, reduced atherosclerotic plaque size, cholesterol crystal load and promoted plaque regression even under continuing Western diet. CD solubilized CCs and promoted cholesterylester and oxysterol production in macrophages leading to liver X receptor (LXR)-mediated transcriptional reprogramming. CD increased cholesterol efflux from macrophages and substantially augmented reverse cholesterol transport in vivo. Furthermore, CD reduced proinflammatory cytokines in vivo and decreased macrophage responsiveness towards TLR and inflammasome activation. Since CD treatment in humans is safe and CD beneficially affects key pathogenetic factors in atherogenesis it may thus be used clinically to prevent or treat human atherosclerosis .

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