化学
癌症免疫疗法
免疫系统
癌症研究
巨噬细胞极化
免疫疗法
封锁
癌症
免疫检查点
微生物学
激酶
唾液链球菌
巨噬细胞
细胞毒性T细胞
免疫学
癌细胞
抗原
受体
TLR5型
唾液乳杆菌
癌症疫苗
细胞生物学
幽门螺杆菌
先天免疫系统
腺癌
作者
Xiang Yu,Yingxin Ren,Jinlong Luo,Jiahao Jiang,Lingzhi Wang,Xinyuan Mao,Yutong Wang,Lang Xie,Yijie Xi,Huilin Huang,Cuiyin Zhao,Yanfeng Hu
标识
DOI:10.1016/j.xcrm.2026.102621
摘要
The immunomodulatory function of the gastric microbiota in cancer is poorly understood, partly due to the stomach’s acidic environment and limited microbial colonization. Here, by analyzing 68 paired human gastric cancer (GC) samples, we identify Ligilactobacillus salivarius as a commensal bacterium depleted in tumors but enriched in immune checkpoint blockade (ICB) responders. Oral administration of L. salivarius enhances anti-PD-1 efficacy in multiple GC mouse models by promoting pro-inflammatory macrophage activation. Mechanistically, bacterial extracellular vesicles (bEVs) derived from L. salivarius deliver 2,3-bisphosphoglycerate-dependent phosphoglycerate mutase (2,3-BdpM) to tumors, where it activates formyl peptide receptor 1 (FPR1) on macrophages, triggering mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) signaling. Moreover, 2,3-BdpM augments the cytotoxic activity of chimeric antigen receptor (CAR)-Claudin18.2 + macrophages in an FPR1-dependent manner. These findings describe a microbial-macrophage axis that enhances GC immunotherapy and highlights the translational potential of orally deliverable microbial adjuvants. • Intratumoral reduction of L. salivarius correlates with GC immunotherapy efficacy • bEVs derived from L. salivarius enhance immunotherapy efficacy in GC mouse models • 2,3-BdpM in bEV triggers pro-inflammatory macrophage remodeling via FPR1 • The cytotoxicity of CAR-Claudin18.2 + macrophages was amplified with 2,3-BdpM alone Yu et al. identify Ligilactobacillus salivarius as a gastric commensal enriched in immunotherapy responders. Oral administration enhances anti-PD-1 efficacy by delivering 2,3-bisphosphoglycerate-dependent phosphoglycerate mutase (2,3-BdpM) via bacterial extracellular vesicles (bEVs) to activate pro-inflammatory macrophages through formyl peptide receptor 1 (FPR1), revealing a microbial-macrophage axis that potentiates gastric cancer immunotherapy.
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