Salter Brittany M, Sehmi Roma
CardioRespiratory Research Group, Department of Medicine, McMaster University, Hamilton, ON, Canada.
CardioRespiratory Research Group, Department of Medicine, McMaster University, Hamilton, ON, Canada.
Chest. 2017 Aug;152(2):410-416. doi: 10.1016/j.chest.2017.01.021. Epub 2017 Jan 24.
Airway eosinophilia is a hallmark of allergic asthma, and understanding mechanisms that promote increases in lung eosinophil numbers is important for effective pharmacotherapeutic development. It has become evident that expansion of hematopoietic compartments in the bone marrow (BM) promotes differentiation and trafficking of mature eosinophils to the airways. Hematopoietic progenitor cells egress the BM and home to the lungs, where in situ differentiation within the tissue provides an ongoing source of proinflammatory cells. In addition, hematopoietic progenitor cells in the airways can respond to locally derived alarmins to produce a panoply of cytokines, thereby themselves acting as effector proinflammatory cells that potentiate type 2 responses in eosinophilic asthma. In this review, we provide evidence for these findings and discuss novel targets for modulating eosinophilopoietic processes, migration, and effector function of precursor cells.
气道嗜酸性粒细胞增多是过敏性哮喘的一个标志，了解促进肺嗜酸性粒细胞数量增加的机制对于有效的药物治疗开发很重要。很明显，骨髓（BM）中造血区室的扩张促进成熟嗜酸性粒细胞向气道的分化和转运。造血祖细胞离开骨髓并归巢到肺部，在那里组织内的原位分化提供了持续的促炎细胞来源。此外，气道中的造血祖细胞可以对局部产生的警报素作出反应，产生一系列细胞因子，从而自身充当效应促炎细胞，增强嗜酸性粒细胞性哮喘中的2型反应。在这篇综述中，我们为这些发现提供了证据，并讨论了调节嗜酸性粒细胞生成过程、前体细胞迁移和效应功能的新靶点。
