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BisDemethoxyCurcumin (BDC) loaded H-Ferritin-Nanocages Mediate Regulation of inflammation in Alzheimer’s Disease Patients

ABSTRACT: BisDemethoxyCurcumin (BDC) loaded H-Ferritin-Nanocages Mediate Regulation of inflammation in Alzheimer’s Disease Patients

PROVIDER: PRJNA839773 | ENA |

REPOSITORIES: ENA

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	SRR19327252_1.fastq.gz	Fastqsanger.gz
	SRR19327252_2.fastq.gz	Fastqsanger.gz
	SRR19327253_1.fastq.gz	Fastqsanger.gz
	SRR19327253_2.fastq.gz	Fastqsanger.gz
	SRR19327254_1.fastq.gz	Fastqsanger.gz

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BisDemethoxyCurcumin (BDC) loaded H-Ferritin-Nanocages Mediate Regulation of inflammation in Alzheimer’s Disease Patients

Project description:Bisdemethoxycurcumin (BDC) might be inflammation inhibitor in AD. BDC is almost insoluble in water, poorly absorbed by the organism, and rapidly degraded. We developed a nanoformulation of BDC based on H-Ferritin nanocages (HFn).

2022-09-04 | GSE203408 | GEO

Bisdemethoxycurcumin (BDC)-Loaded H-Ferritin-Nanocages Mediate the Regulation of Inflammation in Alzheimer's Disease Patients.

Project description:BackgroundBisdemethoxycurcumin (BDC) might be an inflammation inhibitor in Alzheimer's Disease (AD). However, BDC is almost insoluble in water, poorly absorbed by the organism, and degrades rapidly. We thus developed a new nanoformulation of BDC based on H-Ferritin nanocages (BDC-HFn).MethodsWe tested the BDC-HFn solubility, stability, and ability to cross a blood-brain barrier (BBB) model. We tested the effect of BDC-HFn on AD and control (CTR) PBMCs to evaluate the transcriptomic profile by RNA-seq.ResultsWe developed a nanoformulation with a diameter of 12 nm to improve the solubility and stability. The comparison of the transcriptomics analyses between AD patients before and after BDC-HFn treatment showed a major number of DEG (2517). The pathway analysis showed that chemokines and macrophages activation differed between AD patients and controls after BDC-HFn treatment. BDC-HFn binds endothelial cells from the cerebral cortex and crosses through a BBB in vitro model.ConclusionsOur data showed how BDC-Hfn could improve the stability of BDC. Significant differences in genes associated with inflammation between the same patients before and after BDC-Hfn treatment have been found. Inflammatory genes that are upregulated between AD and CTR after BDC-HFn treatment are converted and downregulated, suggesting a possible therapeutic approach.

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Transtriptome analysis of bone marrow-derived neutrophils after ferritin injection

Project description:How ferritin regulates neutrophil leukocyte function remains unknown. To address this question, we injected mice with ferritin. bone marrow-derived neutrophils (BMDN) were isolated by density gradient centrifugation. Then we displayed RNA-seq of isolated BMDNs.

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Alarmin-loaded extracellular lipid droplets induce airway neutrophil infiltration during type 2 inflammation

Project description:Group 2 innate lymphoid cells (ILC2s) play a crucial role in allergic diseases by coordinating a complex network of various effector cell lineages involved in type 2 inflammation. However, their function in regulating airway neutrophil infiltration, a deleterious symptom of severe asthma, remains unknown. Here, we observed ILC2-dependent neutrophil accumulation in the bronchoalveolar lavage fluid (BALF) of allergic mice models. Chromatography followed by proteomics analysis identified the alarmin high mobility group box-1 (HMGB1) in the supernatant of lung ILC2s initiated neutrophil chemotaxis. Genetic perturbation of Hmgb1 in ILC2s reduced BALF neutrophil numbers and alleviated airway inflammation. HMGB1 was loaded onto the membrane of lipid droplets (LDs) released from activated lung ILC2s. Genetic inhibition of LD accumulation in ILC2s significantly decreased extracellular HMGB1 abundance and BALF neutrophil infiltration. These findings unveil a previously uncharacterized extracellular LD-mediated immune signaling delivery pathway by which ILC2s regulate airway neutrophil infiltration during allergic inflammation.

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Alarmin-loaded extracellular lipid droplets induce airway neutrophil infiltration during type 2 inflammation

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The Hyphal Associated Adhesin and Invasin Als3 of Candida albicans Mediates Iron Acquisition from Host Ferritin

Project description:Iron sequestration by host iron-binding proteins is an important mechanism of resistance to microbial infections. Inside oral epithelial cells, iron is stored within the ferritin, and is therefore usually not accessible to pathogenic microbes. We observed that the ferritin concentration within oral epithelial cells was directly related to their susceptibility to damage by the human pathogenic fungus Candida albicans. Thus, we hypothesized that host ferritin may be used as an iron source by this organism. A screen of C. albicans mutants lacking components of each of the three iron acquisition systems revealed that only the reductive pathway is involved in iron utilization from ferritin by this organism. Transcriptional profiling of wild-type and hyphal-defective C. albicans strains suggested that the C. albicans invasin-like protein Als3 plays a role in ferritin binding.

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Glial ferritin maintains self-renewal and proliferation of neural stem cells by supplying iron in Drosophila

Project description:Stem cell niche is critical for regulating the behavior of stem cells. Drosophila neural stem cells (Neuroblasts, NBs) are encased by glial niche cells closely, but it still remains unclear whether glial niche cells can regulate the self-renewal and differentiation of NBs. Here we show that ferritin produced by glia, cooperates with Zip13 to transport iron into NBs for the energy production, which is essential to the self-renewal and proliferation of NBs. The knockdown of glial ferritin encoding genes causes energy shortage in NBs, which leads to the low proliferation and premature differentiation of NBs. Moreover, the level of glial ferritin production is affected by the status of NBs, establishing a bicellular iron homeostasis. In this study, we demonstrate that glial cells are indispensable to maintain the self-renewal of NBs, unveiling a novel role of the NB glial niche during brain development.

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Critical Role of Ferritin-Mediated Iron Homeostasis in the Maintenance of Hematopoietic Stem Cells and Leukemia Stem Cells

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