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ACTG A5258 Clinical administration of chloroquine to patients with untreated chronic HIV infection to reduce immune activation

ABSTRACT: ACTG A5258, we asked whether chloroquine could reduce the immune activation in HIV infection posited to be driven by microbial TLR agonists, such as bacterial elements translocated from the gut and HIV-1 RNAs . We anticipate that blocking this activation pathway might interfere with events in pathogenesis leading to AIDS- and non-AIDS-related clinical manifestations of HIV disease.

ORGANISM(S): Homo sapiens

PROVIDER: GSE71063 | GEO | 2016/07/15

SECONDARY ACCESSION(S): PRJNA290206

REPOSITORIES: GEO

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ACTG A5258 Clinical administration of chloroquine to patients with untreated chronic HIV infection to reduce immune activation

Project description:ACTG A5258, we asked whether chloroquine could reduce the immune activation in HIV infection posited to be driven by microbial TLR agonists, such as bacterial elements translocated from the gut and HIV-1 RNAs . We anticipate that blocking this activation pathway might interfere with events in pathogenesis leading to AIDS- and non-AIDS-related clinical manifestations of HIV disease. Blood samples were taken from 20 individuals at week 0 (before treatement) and week 12. 10 individuals received chloroquine 250mg orally and 10 individuals received placebo.

2016-07-15 | E-GEOD-71063 | biostudies-arrayexpress

ACTG A5258 Clinical administration of chloroquine to HIV-infected patients receiving antiretroviral therapy to reduce immune activation

2016-07-15 | E-GEOD-71064 | biostudies-arrayexpress

ACTG A5258 Clinical administration of chloroquine to HIV-infected patients receiving antiretroviral therapy to reduce immune activation

2016-07-15 | GSE71064 | GEO

Potentiation of glucocorticoid signaling by chloroquine via inhibition of lysosomes

Project description:Anti-malaria drug chloroquine has been used as an anti-inflammatory agent for treating systemic lupus erythematosus and rheumatoid arthritis, without clear mechanism of action. Here we report that chloroquine potently inhibits the expression of proinflammatory cytokines through transrepression of glucocorticoid receptor (GR). Instead of direct binding to GR, chloroquine synergistically activates glucocorticoid signaling via inhibition of lysosomal functions. In mouse collagen induced arthritis model, chloroquine synergizes the therapeutic effects of glucocorticoid. Lysosomal inhibition by bafilomycin A1, an inhibitor of V-type ATPase, or by knockdown of transcription factor EB (TFEB), a master activator of lysosomal biogenesis, mimics the effects of chloroquine. These results reveal an unexpected regulation of glucocorticoid signaling by lysosomes and provide a mechanistic basis for treating inflammation and autoimmune diseases by combination of glucocorticoids and lysosomal inhibitors.

2012-01-18 | GSE24579 | GEO

Potentiation of glucocorticoid signaling by chloroquine via inhibition of lysosomes

2012-01-18 | E-GEOD-24579 | biostudies-arrayexpress

Chloroquine Target Identification with MS-CETSA

Project description:ITDR MS-CETSA was conducted on chloroquine-treated live parasites and lysate of P. falciparum trophozoites in order to identify potential drug protein targets.

2023-12-11 | PXD046662 | Pride

Transcriptomic analysis to identify genes associated with chloroquine-mediated radiosensitization of glioblastoma stem cells

Project description:Tumour suppressor p53 regulates hundreds of genes by either activating or repressing their transcription. p53-dependent transcription is activated by stress factors such as DNA damage, reactive oxygen species, hypoxia or oncogenic signaling. Lysosomotropic agent and DNA intercalating agent chloroquine has been implicated in sensitizing glioblastoma to radiation via p53 pathway. This study evaluates the effects of chloroquine in glioblastoma stem cells differing for the status of TP53 by using an integrated approach encompassing in vitro, in vivo and in silico methodologies to characterize the impacts of chloroquine on cell vitality, tumor-propagating capacity and gene expression. We used microarrays to identify the genes whose expression is influenced by DNA intercalator chloroquine (ClQ) in glioblastoma stem cells expressing wild type p53 (line #993), mutant p53 (line G112) or a p53 null line #1095. To compare chloroquine-associated transcriptomic changes with those induced by ionizing radiation (IR), samples of IR-treated line #993 ("#993_IR") were analyzed in parallel with ClQ-treated samples ("993_ClQ").

2023-08-04 | GSE225191 | GEO

Chloroquine enhances the effectiveness of 5 Fluorouracil in esophageal squamous cell carcinoma via activation of p53 signaling

Project description:To investigate the molecular mechanisms of chloroquine, 5 Fluorouracil, and their combination in ESCC cell line TE11

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RNA-seq of human cell line U2OS treated with chloroquine, amodiaquine and BMH-21

Project description:Ribosome biogenesis has emerged as a potential target for cancer therapy. We have characterize a new biological activity of the antimalarial drug amodiaquine as a inhibitor of ribosome biogenesis. Interestingly, amodiaquine retains the autophagy inhibitory activity of its analog chloroquine, but in addition, displays properties of the ribosome biogenesis inhibitor BMH-21. We performed a RNAseq analysis to identify shared and unique mechanisms of action among these drugs. Gene expression was profiled in U2OS cell line, using 24 samples divided in 4 treatment groups: Untreated, Amodiaquine, Chloroquine and BMH-21, incubated with compounds for 12 hours.

2019-09-01 | E-MTAB-7616 | biostudies-arrayexpress

Transcription profiling of female Anopheles gambiae mosquitoes blood fed on mice infected with P. berghei and treated with chloroquine or untreated

Project description:The effect of chloroquine on mosquitoes transcript abundance was assayed by comparing gene expression between mosquitoes fed on a blood meal containing 50 mg/Kg of chloroquine and those that had fed on a normal blood meal. Pools of 50 midguts were dissected and were hybridize with MMC1 (or 20K) microarrays. <br><br>Anopheles gambiae female mosquitoes were blood fed on BALB/c mice infected with P. berghei and intraperitonally pre-treated with 50 mg/kg of chloroquine. As controls, mosquitoes were blood fed on untreated P. berghei infected mice.<br><br>Mosquitoes were collected 24 hours post-blood feeding and pools of 50 midguts were dissected and processed for hybridization with MMC1 (or 20K) microarrays.Two different biological experiments were performed for each treatment.

2007-10-12 | E-MEXP-1201 | biostudies-arrayexpress

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