Why Chronic Inflammation Persists: The "Broken" Epoxy-Oxylipin Cycle скачать в хорошем качестве

Why Chronic Inflammation Persists: The "Broken" Epoxy-Oxylipin Cycle

A new Nature study identifies a biological "logic gate" that resolves inflammation. We break down how sEH inhibitors prevent monocyte transitioning by modulating the p38 MAPK pathway. The Deep Dive In this episode of SciPulse, we analyze the paper "Epoxy-oxylipins direct monocyte fate in inflammatory resolution in humans" (Nature Communications). While acute inflammation is a necessary defense, its failure to resolve leads to chronic disease. This research maps a previously unknown "resolution architecture" involving cytochrome P450-derived epoxy-oxylipins. We dissect the methodology, where researchers used an intradermal UV-killed E. coli model to track immune response dynamics. The core finding reveals a specific computation within the immune system: the transition of Classical Monocytes to pro-inflammatory Intermediate Monocytes is gated by p38 MAPK signaling. The study demonstrates that the small molecule inhibitor GSK2256294 effectively blocks the soluble epoxide hydrolase (sEH) enzyme. This blockade elevates levels of 12,13-EpOME, effectively "switching off" the differentiation signal and reducing tissue CD4 T-cell accumulation. Academic Integrity: This episode is a summary of peer-reviewed research for educational purposes. It is not medical advice. The detailed mechanisms discussed (specifically GSK2256294 and p38 MAPK interactions) should be reviewed in the original source material. Original Paper: https://www.nature.com/articles/s4146... (Alternate Source: Epoxy-oxylipins direct monocyte fate in inflammatory resolution in humans) #SciPulse #Immunology #Biochemistry #MechanismOfAction #CytochromeP450 #EpoxyOxylipins #sEHInhibitor #SystemsBiology #NatureCommunications #ScientificResearch #MedicalScience #Monocytes #p38MAPK