Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis [IEC bulk RNA-seq]

Necrotizing enterocolitis (NEC) is a prevalent pediatric emergency characterized by the sudden onset of intestinal ischemia and necrosis resulting from hyperinflammation.The interactions between the bile acid receptor FXR with gut microbiota and mucosal immunity in early postnatal life, and its exact role in the pathogenesis of NEC, are unknown.Here we analyze the role of FXR in IECs under NEC. IECs (EpCAM+CD45-) from Fxrfl/fl naive, FxrIEC naive, Fxrfl/fl NEC and FxrIEC NEC pups were sorted via BD FACS. Sorted cells were subjected to bulk RNA-seq坏死性小肠结肠炎（necrotizing enterocolitis, NEC）是一种高发的儿科急症，以过度炎症反应介导的肠道缺血与坏死突发发作为特征。目前，出生后早期胆汁酸受体FXR（farnesoid X receptor, FXR）与肠道菌群、黏膜免疫系统的相互作用，及其在NEC发病机制中的确切作用仍未明确。本研究旨在分析NEC状态下肠上皮细胞（intestinal epithelial cells, IECs）中FXR的功能。研究人员通过BD流式细胞分选仪（BD fluorescence-activated cell sorting, BD FACS），从未造模的Fxrfl/fl幼崽、未造模的FxrIEC幼崽、构建NEC模型的Fxrfl/fl幼崽以及构建NEC模型的FxrIEC幼崽中，分选得到EpCAM+CD45-表型的肠上皮细胞。后续将对分选获得的细胞进行批量RNA测序（bulk RNA-seq）。