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#inflammasome

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Why do preterm neonates struggle to control sepsis?

“This study provides insight into how Krüppel-like factor 2 (KLF2) is involved” and shows that “KLF2 is a promising target in successfully treating newborns with sepsis.”

#preLight from Sydney Call & Sahan Senanayaka #ImmunobiologyUA ! ⬇️ 👀

👉 prelights.biologists.com/highl

preLightsNeutrophil KLF2 regulates inflammasome-dependent neonatal mortality from endotoxemia - preLightsWhy do preterm neonates struggle to control sepsis?

'Here, we show that Arachidonic Acid inhibits the NLRP3 inflammasome, through a PLC-JNK-dependent mechanism, to supress IL-1β production under physiological conditions. This provides a mechanistic basis for how dietary manipulation such as fasting influences the inflammatory state and is likely to be critical for reducing the metaflammation underpinning many diseases induced by the Western Diet.'
#Immunology #Inflammation #inflammasome #Metabolism

cell.com/cell-reports/fulltext

"Inflammasome-mediated caspase-1 activation facilitates innate immune control of Plasmodium in the liver, thereby limiting the incidence and severity of clinical malaria. However, caspase-1 processing occurs incompletely in both mouse and human hepatocytes and precludes the generation of mature IL-1β or IL-18, unlike in other cells. Why this is so or how it impacts Plasmodium control in the liver has remained unknown."
#Malaria #inflammasome

journals.aai.org/jimmunol/arti

American Association of ImmunologistsInherently Reduced Expression of ASC Restricts Caspase-1 Processing in Hepatocytes and Promotes Plasmodium InfectionKey Points. Incomplete caspase-1 processing in hepatocytes is due to lower expression of ASC.Enhancing ASC expression resulted in complete caspase-1 processing

`Through unbiased analyses of #RNA and protein profiles in #Inositol polyphosphate-5-phosphatase D (INPP5D) -disrupted iPSC-derived human #microglia, we find that reduction in INPP5D activity is associated with molecular profiles consistent with disrupted #autophagy and #inflammasome activation.. findings provide insights into the molecular mechanisms underlying microglia-mediated processes in #AD and highlight the inflammasome as a potential #therapeutic target`

nature.com/articles/s41467-023

NatureINPP5D regulates inflammasome activation in human microglia - Nature CommunicationsINPP5D/SHIP1 is a microglial-expressed gene that has been associated with Alzheimer’s disease through genetic studies. This study reveals that reduction in INPP5D activity induces activation of the NLRP3-inflammasome in human microglia.

'Gefitinib (GF), the tyrosine kinase inhibitor (TKI) targeting epidermal growth factor receptor, initiates lung #inflammation through the NLR family pyrin domain containing 3 (NLRP3) inflammasome. However, the molecular targets and mechanisms underlying the inflammatory action of GF remain unknown. In this study, we identified mitochondrial Src family kinases (mSFKs) as key determinants of GF-induced #NLRP3 #inflammasome activation.'

journals.aai.org/jimmunol/arti

American Association of ImmunologistsNLRP3 Inflammasome Works as a Sensor for Detecting Hypoactivity of the Mitochondrial Src Family KinasesKey Points. The tyrosine kinase inhibitors (TKIs) act as agonists for the NLRP3 inflammasome.The TKIs exhibit off-target activity against c-Src, Fgr, and Fyn.Hy

Congratulations to my friend at the Australian National University Professor Si Ming Man, the recipient of the 2022 Frank Fenner Prize for Life Scientist of the Year at the PM prize in Australia. He has been awarded his prestigious prize for his work on #inflammasome and #bacteria infection. Very well deserved for his groundbreaking work and wonderful recipient. facebook.com/IndustryGovAu/

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