Yi Jia-Xuan, Sun Ze-Yu, Liu Peng, Wang Yu-Hang, Liu Hui, Lv Qing-Yu, Kong De-Cong, Huang Wen-Hua, Ren Yu-Hao, Li Qian, Jiang Yong-Qiang, Li Jing, Jiang Hua
College of Biological Science and Food Engineering, Southwest Forestry University, Kunming, Yunnan, China.
State Key Laboratory of Pathogen and Biosecurity, Academy of Military Medical Sciences, Beijing, China.
Cell Death Discov. 2024 Oct 1;10(1):423. doi: 10.1038/s41420-024-02189-8.
IL-1β represents an important inflammatory factor involved in the host response against GBS infection. Prior research has suggested a potential involvement of IL-1β in the process of ferroptosis. However, the relationship between IL-1β and ferroptosis in the context of anti-GBS infection remains uncertain. This research demonstrates that the occurrence of ferroptosis is essential for the host's defense against GBS infection in a mouse model of abdominal infection, with peritoneal macrophages identified as the primary cells undergoing ferroptosis. Further research indicates that IL-1β induces lipid oxidation in macrophages through the upregulation of pathways related to lipid oxidation. Concurrently, IL-1β is not only involved in the initiation of ferroptosis in macrophages, but its production is intricately linked to the onset of ferroptosis. Ultimately, we posit that ferroptosis acts as a crucial initiating factor in the host response to GBS infection, with IL-1β playing a significant role in the resistance to infection by serving as a key inducer of ferroptosis.
白细胞介素-1β（IL-1β）是参与宿主对B族链球菌（GBS）感染反应的一种重要炎症因子。先前的研究表明IL-1β可能参与铁死亡过程。然而，在抗GBS感染的背景下，IL-1β与铁死亡之间的关系仍不明确。本研究表明，在腹部感染小鼠模型中，铁死亡的发生对于宿主抵御GBS感染至关重要，腹膜巨噬细胞被确定为发生铁死亡的主要细胞。进一步研究表明，IL-1β通过上调与脂质氧化相关的途径诱导巨噬细胞中的脂质氧化。同时，IL-1β不仅参与巨噬细胞中铁死亡的启动，其产生还与铁死亡的发生密切相关。最终，我们认为铁死亡是宿主对GBS感染反应中的关键起始因素，而IL-1β作为铁死亡的关键诱导剂，在抗感染中发挥着重要作用。
