Unveiling the crucial role of ferroptosis in host resistance to streptococcus agalactiae infection.

IF 6.1 2区生物学 Q1 CELL BIOLOGY

Cell Death Discovery Pub Date : 2024-10-01 DOI:10.1038/s41420-024-02189-8

Jia-Xuan Yi, Ze-Yu Sun, Peng Liu, Yu-Hang Wang, Hui Liu, Qing-Yu Lv, De-Cong Kong, Wen-Hua Huang, Yu-Hao Ren, Qian Li, Yong-Qiang Jiang, Jing Li, Hua Jiang

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Abstract

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.

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揭示铁蛋白沉积在宿主抵抗无乳链球菌感染中的关键作用。

IL-1β 是一种重要的炎症因子，参与宿主对 GBS 感染的反应。先前的研究表明，IL-1β 可能参与了铁粒体形成过程。然而，在抗 GBS 感染的背景下，IL-1β 与高铁血症之间的关系仍不确定。这项研究表明，在小鼠腹腔感染模型中，铁卟啉沉积的发生对于宿主抵御 GBS 感染至关重要，腹腔巨噬细胞被确定为发生铁卟啉沉积的主要细胞。进一步的研究表明，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 不仅参与了巨噬细胞铁蜕变的启动，而且其产生与铁蜕变的发生有着错综复杂的联系。最终，我们认为铁蜕变是宿主应对 GBS 感染的关键启动因子，IL-1β 作为铁蜕变的关键诱导因子在抗感染中发挥着重要作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cell Death Discovery Biochemistry, Genetics and Molecular Biology-Cell Biology

CiteScore

8.30

自引率

1.40%

发文量

468

审稿时长

9 weeks

期刊介绍： Cell Death Discovery is a multidisciplinary, international, online-only, open access journal, dedicated to publishing research at the intersection of medicine with biochemistry, pharmacology, immunology, cell biology and cell death, provided it is scientifically sound. The unrestricted access to research findings in Cell Death Discovery will foster a dynamic and highly productive dialogue between basic scientists and clinicians, as well as researchers in industry with a focus on cancer, neurobiology and inflammation research. As an official journal of the Cell Death Differentiation Association (ADMC), Cell Death Discovery will build upon the success of Cell Death & Differentiation and Cell Death & Disease in publishing important peer-reviewed original research, timely reviews and editorial commentary. Cell Death Discovery is committed to increasing the reproducibility of research. To this end, in conjunction with its sister journals Cell Death & Differentiation and Cell Death & Disease, Cell Death Discovery provides a unique forum for scientists as well as clinicians and members of the pharmaceutical and biotechnical industry. It is committed to the rapid publication of high quality original papers that relate to these subjects, together with topical, usually solicited, reviews, editorial correspondence and occasional commentaries on controversial and scientifically informative issues.