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<p>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 <i>Candida albicans</i> (<i>C. albicans</i>) infection model, we demonstrated for the first time that disruption of <i>Fhl2</i> 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 <i>Fhl2</i>-deficient mice. In conclusion, FHL2 regulated emergency myelopoiesis in response to <i>C. albicans</i>, affecting the host’s defense against pathogens.</p>

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FHL2 deficiency aggravates Candida albicans infection through decreased myelopoiesis

  • 期刊论文

  • 发表日期：

    2025年1月8日

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  • 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

摘要

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.