Dysregulated hematopoiesis in bone marrow marks severe COVID-19.
Xin WangYanling WenXiaowei XieYang LiuXiaohua TanQingxian CaiYawen ZhangLin ChengGang XuShengyuan ZhangHaiyan WangLanlan WeiXian TangFurong QiJuanjuan ZhaoJing YuanLei LiuPing ZhuFlorent GinhouxShuye ZhangTao ChengZheng ZhangPublished in: Cell discovery (2021)
Severe coronavirus disease 2019 (COVID-19) is often indicated by lymphopenia and increased myelopoiesis; however, the underlying mechanism is still unclear, especially the alteration of hematopoiesis. It is important to explore to what extent and how hematopoietic stem cells contribute to the impairment of peripheral lymphoid and myeloid compartments in COVID-19 patients. In this study, we used single-cell RNA sequencing to assess bone marrow mononuclear cells from COVID-19 patients with peripheral blood mononuclear cells as control. The results showed that the hematopoietic stem cells in these patients were mainly in the G1 phase and prone to apoptosis, with immune activation and anti-viral responses. Importantly, a significant accumulation of immature myeloid progenitors and a dramatic reduction of lymphoid progenitors in severe cases were identified, along with the up-regulation of transcription factors (such as SPI1, LMO4, ETS2, FLI1, and GATA2) that are important for the hematopoietic stem cell or multipotent progenitor to differentiate into downstream progenitors. Our results indicate a dysregulated hematopoiesis in patients with severe COVID-19.
Keyphrases
- coronavirus disease
- bone marrow
- sars cov
- stem cells
- hematopoietic stem cell
- transcription factor
- single cell
- mesenchymal stem cells
- respiratory syndrome coronavirus
- early onset
- end stage renal disease
- dendritic cells
- newly diagnosed
- ejection fraction
- prognostic factors
- drug induced
- acute myeloid leukemia
- chronic kidney disease
- cell death
- immune response
- peripheral blood
- cell therapy
- endoplasmic reticulum stress
- cell cycle arrest
- peritoneal dialysis
- patient reported
- cell fate