MetaboLightsapplication/xmlftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS12891/m_MTBLS12891_LC-MS_alternating_reverse-phase_metabolite_profiling_v2_maf.tsvftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS12891/i_Investigation.txtftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS12891/s_MTBLS12891.txtftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS12891/a_MTBLS12891_LC-MS_alternating_reverse-phase_metabolite_profiling.txtprimaryOK200ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS12891intestinesmass spectrometry assay<p>Using LipidSearch software to perform lipid identification. The main parameters were</p><p>set as follows: precursor tolerance: 5 ppm, product tolerance: 5 ppm, product ion threshold:</p><p>5%.</p><p>Lipids were extracted according to MTBE method. Briefly, a 200-μL volume of water was added to 30 mg sample and vortexed for 5 s. Subsequently, 240 μL of precooling methanol was added and the mixture vortexed for 30 s. After that, 800 μL of MTBE was added and the mixture was ultrasound 20 min at 4 followed by sitting still for 30 min at room temperature. The solution was centrifuged at 14000g for 15min at 10 and the upper organic solvent layer was obtained and dried under nitrogen.</p>Mus musculus<p>Raw data were obtained by LipidSearch software (*.raw format). Preprocessing steps such as peak alignment, peak identification, and peak extraction are performed on lipid molecules and internal standard lipid molecules to get data matrix of mass to charge ratio</p><p>(m/z) , retention time (rt) and peak intensity et al.</p><p>All peak intensities were batch normalized to the total spectral intensity for comparing</p><p>the data of different orders of magnitude.</p>Group15625599188@163.comhttps://www.ebi.ac.uk/metabolights/MTBLS12891<p>Four days after NEC induction of mouse intestinal cells, intestinal tissue was collected and subjected to gradient centrifugation to isolate intestinal ILC3 cells. The collected cell pellets were stored at -80°C and sent to Kidiou Company for testing.</p>MetaboLightsPublicMetabolomicsLiquid Chromatography MS - alternating - reverse phaseILC3phosphatidylcholineNECATG5<p>The sample was separated using the UHPLC Nexera LC-30A ultra-high performance liquid chromatography system. C18 chromatographic column was used with a column temperature of 45 and a flow rate of 300 μL/min. The mobile phase consisted of solvent A: acetonitrile-water solution (acetonitrile:water=6:4,v/v) and solvent B: acetonitrile-isopropanol solution (acetonitrile:isopropanol = 1:9, v/v). The gradient elution program was as follows: 0-2 min, B was maintained at 30%; 2-25 min, B linearly increased from 30% to 100%; 25-35min, B was maintained at 30%. Throughout the entire analysis process, the samples were kept in an autosampler at 10 to prevent any impact from fluctuations in the instrument detection signal. To avoid any systematic errors, the samples were analyzed in a random order.</p>Blocking NKp46-CCR6-ILC3 autophagy alleviates necrotizing enterocolitis by restoring energy metabolism balance.ILC3phosphatidylcholineNECATG5School of Basic Medicine, Southern Medical University, GuangzhouJunyu He<p>Mass spectra was acquired by Q-Exactive Plus in positive and negative mode, respectively. ESI parameters were optimized and preset for all measurements as follows: Source temperature, 300 °C; Capillary Temp, 350 °C, the ion spray voltage was set at 3000V, S-Lens RF Level was set at 50% and the scan range of the instruments was set at m/z 200–1800.</p><p>The mass-to-charge ratio (m/z) of lipid molecules and lipid fragments is collected using</p><p>the following method: After each full scan, 10 fragment spectra (MS2 scan, HCD) are</p><p>collected. The resolution of MS1 is 70,000 at m/z 200, while the resolution of MS2 is 17,500</p><p>at m/z 200.</p>falseBlocking NKp46-CCR6-ILC3 autophagy alleviates necrotizing enterocolitis by restoring energy metabolism balance<p>Group 3 innate lymphoid cells (ILC3s) play a crucial role in intestinal inflammatory disorders such as necrotizing enterocolitis (NEC) in neonates; however, the mechanisms by which ILC3s contribute to NEC remain unclear. In this study, single-cell transcriptomics, in vivo experiments on T cell-deficient mice, and targeted cell interventions demonstrated that NKp46CCR6 (double-negative, DN) ILC3 autophagy significantly impacts NEC development by regulating intracellular metabolism. Mice lacking ATG5 or treated with autophagy inhibitors exhibited reduced ILC3 abundance and impaired ILC3 function, alleviating NEC. Mechanistically, ATG5 deficiency enhanced fatty acid metabolism while reducing glycolysis. Conversely, inhibiting fatty acid oxidation or supplementing with lactate restored the quantity and functionality of ATG5-deficient DN ILC3s, exacerbating NEC. Lipid metabolism analyses combined with a mouse model of NEC indicated that phosphatidylcholine supplementation alleviated intestinal inflammation by inhibiting DN ILC3 autophagy. Clinically, patients with NEC showed elevated ILC3 levels and significant enrichment of autophagy genes. These findings highlight the importance of DN ILC3 autophagy in metabolic adaptation, suggesting potential strategies for managing NEC.</p>2026-04-122025-08-24MTBLS12891