Plasma essential fatty acid on hospital admission is a marker of COVID-19 disease severity

Scientific Reports, Journal Year: 2023, Volume and Issue: 13(1)

Published: Nov. 3, 2023

It is important for allocation of resources to predict those COVID patients at high risk dying or organ failure. Early signals initiate cellular events host immunity can be derived from essential fatty acid metabolites preceding the cascade proinflammatory signals. Much research has focused on understanding later responses. We assessed if remodelling plasma phospholipid content acids by COVID-19 virus provides early markers potential death and disease severity. Here we show that, hospital admission, infected subjects who survive exhibit higher proportions C20:4n-6 in phospholipids concurrent with marked cytokine elevation compared healthy subjects. In contrast, more than half die this very low C18:2n-6 admission control Moreover, these die, level primary inflammatory indicates limited aberrant stimulation immunity. conclude that infection results fundamental metabolism. mortality, it appears n-6 too stimulate

Language: Английский

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Glucocerebrosidase deficiency leads to neuropathology via cellular immune activation

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2023, Volume and Issue: unknown

Published: Dec. 13, 2023

Abstract Mutations in GBA ( glucosylceramidase beta ), which encodes the lysosomal enzyme glucocerebrosidase (GCase), are strongest genetic risk factor for neurodegenerative disorders Parkinson’s disease (PD) and Lewy body dementia. Recent work has suggested that neuroinflammation may be an important conferred by mutations. We therefore systematically tested contributions of immune-related genes to neuropathology a Drosophila model GCase deficiency. identified target immune factors via RNA-Seq proteomics on heads from GCase-deficient flies, revealed both increased abundance humoral macrophage activation. then manipulated measured their effect head protein aggregates, hallmark disease. Genetic ablation (secreted) did not suppress development aggregation. By contrast, re-expressing Gba1b activated macrophages suppressed aggregation mutants rescued lifespan behavioral deficits. Moreover, reducing substrate glucosylceramide also ameliorated mutant phenotypes. Taken together, our findings show accumulation due deficiency leads activation, turn promotes neuropathology. Author Summary gene largest developing dementia, diseases brain cells die. know system can involved these diseases, mutations cause changes. experiments learn how changes could make more likely Using fruit fly was missing version , we found out inappropriately cells, but secreted proteins, were problems. learned abnormal activation triggered lack function signals or other parts body. would like find next whether get inside harm distance. What matters because it help us prevent cure associated with Treating people might damage brain.

Language: Английский

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Glia-neuron interplay drives circadian glycosphingolipid homeostasis and structural brain plasticity

Neuron, Journal Year: 2022, Volume and Issue: 110(19), P. 3058 - 3060

Published: Oct. 1, 2022

Glia-neuronal interplay is critical for circadian regulation of physiology and behavior. In this issue Neuron, Vaughen et al. identify daily variations glycosphingolipids that depend on glia whose disruption alters proteostasis structural plasticity Drosophila circuits.

Language: Английский

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