巨核细胞
造血
免疫学
生物
血小板生成素
细胞激素风暴
干细胞
祖细胞
病毒学
甲型流感病毒
病毒
医学
细胞生物学
内科学
疾病
2019年冠状病毒病(COVID-19)
传染病(医学专业)
作者
Marcel G. E. Rommel,Lisa Walz,Foteini Fotopoulou,Saskia Kohlscheen,Franziska Schenk,Csaba Miskey,Lacramioara Botezatu,Yvonne Krebs,Iris M. Voelker,Kevin Wittwer,Tim Holland-Letz,Zoltán Ivics,Veronika von Messling,Marieke A.G. Essers,Michael D. Milsom,Christian K. Pfaller,Ute Modlich
出处
期刊:Cell Reports
[Elsevier]
日期:2022-10-01
卷期号:41 (1): 111447-111447
标识
DOI:10.1016/j.celrep.2022.111447
摘要
Summary
Respiratory tract infections are among the deadliest communicable diseases worldwide. Severe cases of viral lung infections are often associated with a cytokine storm and alternating platelet numbers. We report that hematopoietic stem and progenitor cells (HSPCs) sense a non-systemic influenza A virus (IAV) infection via inflammatory cytokines. Irrespective of antiviral treatment or vaccination, at a certain threshold of IAV titer in the lung, CD41-positive hematopoietic stem cells (HSCs) enter the cell cycle while endothelial protein C receptor-positive CD41-negative HSCs remain quiescent. Active CD41-positive HSCs represent the source of megakaryocytes, while their multi-lineage reconstitution potential is reduced. This emergency megakaryopoiesis is thrombopoietin independent and attenuated in IAV-infected interleukin-1 receptor-deficient mice. Newly produced platelets during IAV infection are immature and hyper-reactive. After viral clearance, HSC quiescence is re-established. Our study reveals that non-systemic viral respiratory infection has an acute impact on HSCs via inflammatory cytokines to counteract IAV-induced thrombocytopenia.
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