Division of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA.
Proc Natl Acad Sci U S A. 2013 Apr 9;110(15):6067-72. doi: 10.1073/pnas.1220572110. Epub 2013 Mar 27.
Most in vivo studies of granulocytes draw conclusions about their trafficking based on examination of their steady-state tissue/blood levels, which result from a combination of tissue homing, survival, and egress, rather than direct examination of cellular trafficking. Herein, we developed a unique cell transfer system involving the adoptive transfer of a genetically labeled, bone-marrow-derived unique granulocyte population (eosinophils) into an elicited inflammatory site, the allergic lung. A dual polychromatic FACS-based biomarker-labeling system based on the IL4-eGFP transgene (4get) or Cd45.1 allele was used to track i.v. transferred eosinophils into the airway following allergen or T(H)2-associated stimuli in the lung in multiple mouse strains. The system was amenable to reverse tagging of recipients, thus allowing transfer of nonlabeled eosinophils and competitive tracking of multiple populations of eosinophils in vivo. The half-life of eosinophils in the blood was 3 h, and migration to the lung was dependent upon the dosage of transferred eosinophils, sensitive to pertussis toxin pretreatment, peaked at ∼24 h after adoptive transfer, and revealed a greater than 8-d eosinophil half-life in the lung. Eosinophil migration to the lung was dependent upon recipient IL-5 and IL-13 receptor α1 and donor eosinophil C-C chemokine receptor type 3 (CCR3) and interleukin 1 receptor-like 1 (ST2) in vivo. Taken together, this unique eosinophil transfer system provides an unprecedented opportunity to examine airway eosinophil migration without the need for extensive efforts to acquire donor source and time-consuming genetic crossing and has already been used to identify a long eosinophil half-life in the allergic lung and a definite role for ST2 in regulating eosinophil trafficking.
大多数关于粒细胞的体内研究都是基于其在组织/血液中的稳态水平来推断其迁移情况,这些水平是由组织归巢、存活和迁出共同作用的结果,而不是直接对细胞迁移进行检测。在此,我们开发了一种独特的细胞转移系统,涉及将经过基因标记的、骨髓来源的独特粒细胞群(嗜酸性粒细胞)过继转移到诱发的炎症部位,即过敏性肺。采用基于 IL4-eGFP 转基因(4get)或 Cd45.1 等位基因的双多色流式细胞术(FACS)生物标志物标记系统,在多种小鼠品系中,跟踪经静脉注射转移的嗜酸性粒细胞在肺内过敏原或 T(H)2 相关刺激物作用下进入气道。该系统适用于受体的反向标记,从而允许转移未标记的嗜酸性粒细胞,并在体内对多个嗜酸性粒细胞群体进行竞争性跟踪。嗜酸性粒细胞在血液中的半衰期为 3 小时,向肺的迁移依赖于转移的嗜酸性粒细胞的剂量,对百日咳毒素预处理敏感,在过继转移后约 24 小时达到峰值,并在肺中显示出超过 8 天的嗜酸性粒细胞半衰期。嗜酸性粒细胞向肺的迁移依赖于受体的 IL-5 和 IL-13 受体 α1 以及供体嗜酸性粒细胞 C-C 趋化因子受体 3(CCR3)和白细胞介素 1 受体样 1(ST2)。总之,这种独特的嗜酸性粒细胞转移系统为研究气道嗜酸性粒细胞迁移提供了一个前所未有的机会,而无需花费大量精力获取供体来源和进行耗时的基因交叉,并且已经用于确定过敏性肺中嗜酸性粒细胞的长半衰期和 ST2 在调节嗜酸性粒细胞迁移中的明确作用。