Gottfried Schatz Research Center, Molecular Biology and Biochemistry, Medical University of Graz, Neue Stiftingtalstrasse 6/4, 8010 Graz, Austria.
Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Via Balzaretti 9, 20133 Milan, Italy.
J Proteome Res. 2024 Apr 5;23(4):1506-1518. doi: 10.1021/acs.jproteome.4c00082. Epub 2024 Feb 29.
The metabolic contribution of the small intestine (SI) is still unclear despite recent studies investigating the involvement of single cells in regional differences. Using untargeted proteomics, we identified regional characteristics of the three intestinal tracts of C57BL/6J mice and found that proteins abundant in the mouse ileum correlated with the high ileal expression of the corresponding genes in humans. In the SI of C57BL/6J mice, we also detected an increasing abundance of lysosomal acid lipase (LAL), which is responsible for degrading triacylglycerols and cholesteryl esters within the lysosome. LAL deficiency in patients and mice leads to lipid accumulation, gastrointestinal disturbances, and malabsorption. We previously demonstrated that macrophages massively infiltrated the SI of Lal-deficient (KO) mice, especially in the duodenum. Using untargeted proteomics (ProteomeXchange repository, data identifier PXD048378), we revealed a general inflammatory response and a common lipid-associated macrophage phenotype in all three intestinal segments of Lal KO mice, accompanied by a higher expression of GPNMB and concentrations of circulating sTREM2. However, only duodenal macrophages activated a metabolic switch from lipids to other pathways, which were downregulated in the jejunum and ileum of Lal KO mice. Our results provide new insights into the process of absorption in control mice and possible novel markers of LAL-D and/or systemic inflammation in LAL-D.
尽管最近有研究调查了单个细胞在区域差异中的作用,但小肠(SI)的代谢贡献仍不清楚。我们使用非靶向蛋白质组学方法鉴定了 C57BL/6J 小鼠的三个肠道区域的区域特征,发现小鼠回肠中丰富的蛋白质与人类相应基因在回肠中的高表达相关。在 C57BL/6J 小鼠的 SI 中,我们还检测到溶酶体酸性脂肪酶(LAL)的丰度增加,LAL 负责在溶酶体中降解三酰甘油和胆固醇酯。患者和小鼠中 LAL 的缺乏导致脂质积累、胃肠道紊乱和吸收不良。我们之前证明,巨噬细胞大量浸润 Lal 缺陷(KO)小鼠的 SI,特别是十二指肠。我们使用非靶向蛋白质组学(ProteomeXchange 存储库,数据标识符 PXD048378)揭示了 Lal KO 小鼠所有三个肠道段的普遍炎症反应和常见的与脂质相关的巨噬细胞表型,同时伴随着 GPNMB 的更高表达和循环 sTREM2 的浓度增加。然而,只有十二指肠巨噬细胞激活了从脂质到其他途径的代谢转变,而 Lal KO 小鼠的空肠和回肠中的这些途径则下调。我们的研究结果为对照小鼠的吸收过程提供了新的见解,并为 LAL-D 和/或全身性炎症的 LAL-D 提供了可能的新型标记物。