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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

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Transtriptome analysis of bone marrow-derived neutrophils after ferritin injection

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

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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.

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