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FHL2缺陷通过减少骨髓生成加重白色念珠菌感染。

FHL2 deficiency aggravates Candida albicans infection through decreased myelopoiesis.

作者信息

Gao Rongmei, Chen Kanchao, Wang Yimin, Guo Rongxia, Zhang Xiaoyu, Wu Peng, Wang Weili, Huang Qingxiang, Xie Xuemei, Yang Shangda, Lv Yanling, Ren Qian, Liu Fei, Chen Song, Ma Fengxia, Cheng Tao, Cheng Hui

机构信息

State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, 300020, China.

PUMC Department of Stem Cell and Regenerative Medicine, CAMS Center for Stem Cell Medicine, Tianjin, 300020, China.

出版信息

Sci China Life Sci. 2025 Mar;68(3):722-733. doi: 10.1007/s11427-024-2645-y. Epub 2025 Jan 8.

Abstract

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.

摘要

造血作用是一个精细调节的过程,通过自我更新和分化产生所有血细胞类型,这对维持体内平衡至关重要。急性感染可引发一种称为应急髓系造血的造血反应。在本研究中,我们使用白色念珠菌感染模型,首次证明Fhl2的破坏导致真菌负荷增加、炎症反应加剧和存活率降低。Fhl2缺陷小鼠骨髓中造血干细胞和祖细胞(HSPCs)以及粒细胞数量减少,证明髓系造血和免疫细胞生成受损。总之,FHL2调节针对白色念珠菌的应急髓系造血,影响宿主对病原体的防御。

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