Department of Chemistry, University of Minnesota , 207 Pleasant Street SE, Minneapolis, Minnesota 55455, United States.
Anal Chem. 2013 Nov 19;85(22):10787-96. doi: 10.1021/ac4020098. Epub 2013 Oct 28.
Neutrophils are always surrounded by/interacting with other components of the immune system; however, the current mechanistic understanding of neutrophil function is largely based on how neutrophils respond to a single chemical signal in a simplified environment. Such approaches are unable to recapitulate the in vivo microenvironment; thus, cell behavior may not fully represent the physiological behavior. Herein, we exploit a microfluidic model of the complex in vivo milieu to investigate how cell-cell interactions influence human neutrophil migration and surface marker expression. Neutrophil migration against a bacterially derived chemoattractant (formyl-met-leu-phe, fMLP), with and without preactivation by interleukins (interleukin-2 or interleukin-6), was evaluated in the presence and absence of endothelial support cells. Preactivation by interleukins or interaction with endothelial cells resulted in altered migration rates compared to naïve neutrophils, and migration trajectories deviated from the expected movement toward the fMLP signal. Interestingly, interaction with both interleukins and endothelial cells simultaneously resulted in a slight compensation in the deviation-on endothelial cells, 34.4% of untreated neutrophils moved away from the fMLP signal, while only 15.2 or 22.2% (interleukin-2-or interleukin-6-activated) of preactivated cells moved away from fMLP. Neutrophils interacting with interleukins and/or endothelial cells were still capable of prioritizing the fMLP signal over a competing chemoattractant, leukotriene B4 (LTB4). Fluorescence imaging of individual human neutrophils revealed that neutrophils treated with endothelial-cell-conditioned media showed up-regulation of the surface adhesion molecules cluster determinant 11b and 66b (CD11b and CD66b) upon stimulation. On the other hand, CD11b and CD66b down-regulation was observed in untreated neutrophils. These results leverage single cell analysis to reveal that the interaction between neutrophils and endothelial cells is involved in surface marker regulation and thus chemotaxis of neutrophils. This study brings new knowledge about neutrophil chemotaxis in the context of cell-to-cell communications, yielding both fundamental and therapeutically relevant insight.
中性粒细胞总是被免疫系统的其他成分包围或相互作用;然而,目前对中性粒细胞功能的机制理解在很大程度上是基于中性粒细胞在简化环境中对单个化学信号的反应。这种方法无法重现体内微环境;因此,细胞行为可能无法完全代表生理行为。在这里,我们利用复杂的体内环境的微流控模型来研究细胞-细胞相互作用如何影响人中性粒细胞的迁移和表面标志物表达。在有和没有内皮支持细胞的情况下,评估了中性粒细胞在细菌衍生的趋化因子(甲酰基-甲硫氨酸-亮氨酸-苯丙氨酸,fMLP)作用下的迁移,以及白细胞介素(白细胞介素-2 或白细胞介素-6)预先激活后的迁移。与内皮细胞相互作用或预先激活白细胞介素导致与未激活的中性粒细胞相比,迁移率发生了变化,并且迁移轨迹偏离了向 fMLP 信号的预期运动。有趣的是,与白细胞介素和内皮细胞同时相互作用导致在离开 fMLP 信号方面的轻微补偿,未经处理的中性粒细胞中有 34.4%离开 fMLP 信号,而预先激活的细胞中只有 15.2%或 22.2%(白细胞介素-2 或白细胞介素-6 激活)离开 fMLP。与白细胞介素和/或内皮细胞相互作用的中性粒细胞仍然能够优先选择 fMLP 信号而不是竞争趋化因子白三烯 B4(LTB4)。对单个人类中性粒细胞的荧光成像显示,用内皮细胞条件培养基处理的中性粒细胞在受到刺激时,表面粘附分子簇分化抗原 11b 和 66b(CD11b 和 CD66b)的表达上调。另一方面,在未经处理的中性粒细胞中观察到 CD11b 和 CD66b 的下调。这些结果利用单细胞分析揭示了中性粒细胞与内皮细胞之间的相互作用参与了中性粒细胞表面标志物的调节,从而参与了中性粒细胞的趋化作用。这项研究为中性粒细胞在细胞间通讯背景下的趋化作用提供了新的知识,为基础和治疗相关的见解提供了新的知识。