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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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			Action	DRS
	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.

| S-EPMC9409287 | biostudies-literature

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.

2021-07-09 | GSE179679 | GEO

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.

2024-09-21 | GSE245964 | GEO

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

Project description: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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Project description:Iron is an essential nutrient for humans as well as for pathogens. Hence, its correct distribution at the systemic and cellular level is mandatory for mounting an effective innate immune defense. Here we delved into the role of macrophage-expressed iron storing protein ferritin H (FTH) in immune response against the model intracellular pathogen Salmonella Typhimurium. Mice lacking FTH in the myeloid lineage (LysM-Cre+/+ Fthfl/fl) displayed impaired iron storage capacities in tissue leukocyte compartment, increased levels of labile iron in macrophages and an accelerated macrophage-mediated iron turnover. Without iron supplementation, wildtype (WT) and LysM-Cre+/+ Fthfl/fl animals showed comparable susceptibility to Salmonella infection. Interestingly, iron supplementation rapidly elicited symptoms of cytokine storm and drastically shortened survival of LysM-Cre+/+ Fthfl/fl mice. Mechanistically, we traced this phenotype back to labile iron-mediated hyperactivity of the inflammasome in FTH-deficient macrophages, culminating in excessive IL-1β secretion and secondary triggering of NF-kappaB-dependent inflammatory circuits. Accordingly, bacterial burden and cytokine levels in iron-loaded LysM-Cre+/+ Fthfl/fl mice could be effectively kept at bay by pharmacological inflammasome and IL-1β blockade. These findings point towards a previously unrecognized role of ferritin as an inhibitor of iron-dependent inflammasome activity in macrophages and a checkpoint of systemic innate response.

2021-02-12 | GSE145114 | GEO

Let-7b-5p loaded Mesenchymal Stromal Cell Extracellular Vesicles reduce Pseudomonas-biofilm formation and inflammation in CF Bronchial Epithelial Cells

Project description:Chronic Pseudomas aeruginosa infection in the lung is a common in people with cystic fibrosis (CF). Current therapies for CF fail to eliminate persistent bacterial infections, chronic inflammation, or irreversible lung damage. Our group engineered mesenchymal stromal cell (MSC)-derived extracellular vesicles (EVs) to carry the microRNA let-7b-5p as a dual anti-infective and anti-inflammatory treatment. In a preclinical CF mice model, we found that let-7b-5p-loaded MSC EVs reduced P. aeruginosa burden, immune cells and proinflammatory cytokines in the lungs. This research hypothesized two mechanisms of the observed effects in the mouse model: anti-inflammatory properties of the let-7b-5p-loaded MSC EVs and inhibition of antibiotic-resistant P. aeruginosa biofilm formation in CF airways. Primary human broncial epithelial cells (pHBECs) were exposed to P. aeruginosa and treated with differet MSC EV conditions. The results demonstrated that MSC EVs engineered to contain let-7b-5p effectively blocked the formation of P. aeruginosa biofilms on pHBECs while also reducing P. aeruginosa-induced inflammation by CF-pHBECs.

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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.

2024-07-15 | GSE237124 | GEO

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

Project description:Iron metabolism has emerged as a critical factor in cell viability, both in normal and pathological contexts. However, the intricate relationship between iron metabolism and the maintenance of adult stem cells and cancer stem cells remains incompletely understood. The ferritin complex, responsible for intracellular iron storage and buffering, plays a pivotal role in this process. Our research provides insights into the regulatory role of ferritin-mediated iron homeostasis in hematopoietic stem cells (HSCs).

2024-04-17 | GSE240742 | GEO

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