Center for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, Blood, and Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Center for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, Blood, and Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Cytokine. 2017 Dec;100:11-15. doi: 10.1016/j.cyto.2017.08.015. Epub 2017 Aug 30.
Myeloid cells, including monocytes and macrophages participate in steady state immune homeostasis and help mount the adaptive immune response during infection. The function and production of these cells in sterile inflammation, such as pulmonary hypertension (PH), is understudied. Emerging data indicate that pulmonary inflammation mediated by lung perivascular macrophages is a key pathogenic driver of pulmonary remodeling leading to increased right ventricular systolic pressure (RVSP). However, the origin of these macrophages in pulmonary inflammation is unknown. Inflammatory monocytes, the precursors of pathogenic macrophages, are derived from hematopoietic stem and progenitor cells (HSPC) in the bone marrow and spleen during acute and chronic inflammation. Understanding the role of these organs in monocytopoiesis, and the mechanisms of HSPC proliferation and differentiation in PH are important to discover therapeutic targets curbing inflammation. This review will summarize the current limited knowledge of the origin of lung macrophage subsets and over-production of inflammatory monocytes in PH.
髓系细胞，包括单核细胞和巨噬细胞，参与稳态免疫平衡，并有助于在感染期间引发适应性免疫反应。在无菌性炎症（如肺动脉高压，PH）中，这些细胞的功能和产生尚不清楚。新出现的数据表明，由肺血管周围巨噬细胞介导的肺部炎症是导致右心室收缩压（RVSP）升高的肺重构的关键致病驱动因素。然而，这些巨噬细胞在肺部炎症中的来源尚不清楚。炎性单核细胞是致病性巨噬细胞的前体，在急性和慢性炎症期间，来源于骨髓和脾脏中的造血干细胞和祖细胞（HSPC）。了解这些器官在单核细胞生成中的作用，以及 HSPC 在 PH 中的增殖和分化的机制，对于发现抑制炎症的治疗靶点非常重要。本综述将总结目前关于肺巨噬细胞亚群的来源以及 PH 中炎性单核细胞过度产生的有限知识。
