Sequential binding of CD11a/CD18 and CD11b/CD18 defines neutrophil capture and stable adhesion to Intercellular adhesion molecule-1
Sequential binding of CD11a/CD18 and CD11b/CD18 defines neutrophil capture and stable adhesion to Intercellular adhesion molecule-1
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DOI：
10.1182/blood.v95.3.911.003k36_911_920
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发表时间：
2000-02-01
期刊：
影响因子：
20.3
通讯作者：
Simon, SI
中科院分区：
文献类型：
--
作者：
Hentzen, ER;Neelamegham, S;Simon, SI
在趋化刺激的时间过程中，检测了CD 11 a/CD 18和CD 11b/CD 18对中性粒细胞粘附于细胞间粘附分子（ICAM）-1转染细胞的动力学和强度的相对贡献。在锥板粘度计中剪切嗜中性粒细胞和转染子的悬浮液，并通过双色流式细胞术测量异型聚集体的形成。使用2体碰撞理论计算粘附效率，粘附效率定义为导致捕获的中性粒细胞和靶细胞之间的碰撞比例。ICAM-1表面密度和剪切速率均调节粘附效率，表达约1000个ICAM-1位点/μ m（2）（I-低）的靶细胞在100 s（-1）时以0.15的效率被捕获，在300 s（-1）时降低至零。当ICAM-1表达（I-高）是白细胞介素-1刺激的内皮细胞的8倍时，效率在100 s（-1）时为0.3，并保持高于背景值至900 s（-1）。单独的剪切足以使CD 11 a/CD 18介导的与ICAM-1的粘附，用甲酰-甲硫氨酰-亮氨酰-苯丙氨酸刺激可使通过CD 11 a/CD 18的捕获效率提高4倍。相比之下，CD 11b/CD 18支持该效率的三分之一，但对于在几分钟的剪切和超过5达因/厘米（2）的剪切应力下的聚集体稳定性是必要的。流体动力学主要通过碰撞接触持续时间影响捕获效率，预计成功捕获I-低约为9毫秒，I-高约为4毫秒。这意味着ICAM-1从静息水平增加到发炎内皮上的水平有效地增加了可允许的剪切力，其中可能发生通过β 2-整合素的捕获。神经细胞粘附ICAM-1似乎是一个合作和顺序的过程中，CD 11 a依赖的捕获，然后由CD 11b介导的稳定。(C)2000年，美国血液学会。
The relative contributions of CD11a/CD18 and CD11b/CD18 to the dynamics and strength of neutrophil adhesion to intercellular adhesion molecule (ICAM)-1-transfected cells were examined over the time course of chemotactic stimulation. Suspensions of neutrophils and transfectants were sheared in a cone-plate viscometer, and formation of heterotypic aggregates was measured by 2-color flow cytometry. The 2-body collision theory was used to compute adhesion efficiency, defined as the proportion of collisions between neutrophils and target cells that resulted in capture. ICAM-1 surface density and shear rate both regulated adhesion efficiency, Target cells expressing approximately 1000 ICAM-1 sites/mu m(2)(I-low) were captured with an efficiency of 0.15 at 100 s(-1), which decreased to zero at 300 s(-1). At 8-fold higher ICAM-1 expression (I-high) corresponding to levels measured on interleukin-1-stimulated endothelium, efficiency was 0.3 at 100 s(-1) and remained above background to 900 s(-1) Shear alone was sufficient for CD11a/CD18-mediated adhesion to ICAM-1, and stimulation with formyl-methionyl-leucyl-phenylalanine boosted capture efficiency through CD11a/CD18 by 4-fold. In comparison, CD11b/CD18 supported one third of this efficiency, but was necessary for aggregate stability over several minutes of shear and at shear stresses exceeding 5 dyne/cm(2). Hydrodynamics influenced capture efficiency predominantly through the collisional contact duration, predicted to be approximately 9 milliseconds for successful capture of I-low and 4 milliseconds for I-high The implication is that an increase in ICAM-1 from resting levels to those on inflamed endothelium effectively increases the permissible shear in which capture through beta(2)-integrins may occur. Neutrophil adhesion to ICAM-1 appears to be a cooperative and sequential process of CD11a-dependent capture followed by CD11b-mediated stabilization.(C) 2000 by The American Society of Hematology.