FHL2缺乏通过减少骨髓生成加重白色念珠菌感染。

IF 8 2区 生物学 Q1 BIOLOGY
Science China Life Sciences Pub Date : 2025-03-01 Epub Date: 2025-01-08 DOI:10.1007/s11427-024-2645-y
Rongmei Gao, Kanchao Chen, Yimin Wang, Rongxia Guo, Xiaoyu Zhang, Peng Wu, Weili Wang, Qingxiang Huang, Xuemei Xie, Shangda Yang, Yanling Lv, Qian Ren, Fei Liu, Song Chen, Fengxia Ma, Tao Cheng, Hui Cheng
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引用次数: 0

摘要

造血是一个精细调节的过程,通过自我更新和分化产生所有类型的血细胞,这对维持体内平衡至关重要。急性感染可引起称为紧急骨髓生成的造血反应。在这项研究中,使用白色念珠菌(C. albicans)感染模型,我们首次证明了Fhl2的破坏导致真菌负荷增加,炎症反应增强和生存率降低。骨髓造血功能和免疫细胞生成明显受损,这可以通过fhl2缺陷小鼠骨髓中造血干细胞和祖细胞(HSPCs)和粒细胞数量的减少来证明。综上所述,FHL2调节紧急骨髓生成以应对白色念珠菌,影响宿主对病原体的防御。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
FHL2 deficiency aggravates Candida albicans infection through decreased myelopoiesis.

Hematopoiesis is a finely tuned process that generates all blood cell types through self-renewal and differentiation, which is crucial for maintaining homeostasis. Acute infections can prompt a hematopoietic response known as emergency myelopoiesis. In this study, using a Candida albicans (C. albicans) infection model, we demonstrated for the first time that disruption of Fhl2 led to increased fungal burden, heightened inflammatory response and reduced survival rates. Impaired myeloid hematopoiesis and immune cell production were evident, as proved by the decreased numbers of hematopoietic stem and progenitor cells (HSPCs) and granulocytes in the bone marrow of Fhl2-deficient mice. In conclusion, FHL2 regulated emergency myelopoiesis in response to C. albicans, affecting the host's defense against pathogens.

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来源期刊
CiteScore
15.10
自引率
8.80%
发文量
2907
审稿时长
3.2 months
期刊介绍: Science China Life Sciences is a scholarly journal co-sponsored by the Chinese Academy of Sciences and the National Natural Science Foundation of China, and it is published by Science China Press. The journal is dedicated to publishing high-quality, original research findings in both basic and applied life science research.
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