Jiang Suisui, Yao Sai, Lu Chunyun, Zhou Ying, Gao Tianlin, Liu Shichao, Zhong Feng
Institute of Nutrition and Health, School of Public Health Qingdao University Qingdao Shandong China.
Qingdao Central Hospital University of Health and Rehabilitation Sciences Qingdao Shandong China.
Food Sci Nutr. 2025 Aug 27;13(9):e70871. doi: 10.1002/fsn3.70871. eCollection 2025 Sep.
Radiotherapy, a common method for treating pelvic and abdominal cancer, can easily result in radiation enteritis (RE). The gut microbiota and its metabolites have a crucial role in regulating macrophage polarization and maintaining immune homeostasis. FN041, derived from human milk, can promote M2 polarization while attenuating RE. After FN041 treatment, the crypt depth and goblet cell numbers were significantly improved in RE mice. The levels of Muc2, ZO-1, and Occludin were significantly higher in the FN041 group than in the RE group. FN041 stimulated the polarization of macrophages toward M2 and inhibited the expression of IL-6 and TNF-α in RE mice. Mechanically, FN041 regulated the gut microbiota and metabolites, including key intermediates in phospholipid synthesis such as CDP-DG, prostaglandins, and their phospholipid derivatives (including PI, PE, PA, and PS), which were linked to M2 macrophage polarization. Collectively, FN041 exerts a protective effect against RE by modulating macrophage polarization based on gut microbiota and its metabolites.
放射疗法是治疗盆腔和腹部癌症的常用方法，很容易导致放射性肠炎（RE）。肠道微生物群及其代谢产物在调节巨噬细胞极化和维持免疫稳态方面起着关键作用。源自人乳的FN041可促进M2极化，同时减轻放射性肠炎。在FN041治疗后，放射性肠炎小鼠的隐窝深度和杯状细胞数量显著改善。FN041组中Muc2、ZO-1和闭合蛋白的水平显著高于放射性肠炎组。FN041刺激巨噬细胞向M2极化，并抑制放射性肠炎小鼠中IL-6和TNF-α的表达。从机制上讲，FN041调节肠道微生物群及其代谢产物，包括磷脂合成中的关键中间体，如CDP-DG、前列腺素及其磷脂衍生物（包括PI、PE、PA和PS），这些与M2巨噬细胞极化有关。总体而言，FN041通过基于肠道微生物群及其代谢产物调节巨噬细胞极化，对放射性肠炎发挥保护作用。
