C3a is a chemotaxin for human eosinophils but not for neutrophils. I. C3a stimulation of neutrophils is secondary to eosinophil activation.
C3a is a chemotaxin for human eosinophils but not for neutrophils. I. C3a stimulation of neutrophils is secondary to eosinophil activation.
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DOI：
10.1084/jem.181.6.2119
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发表时间：
1995-06-01
影响因子：
15.3
通讯作者：
Hugli, Tony E.
中科院分区：
文献类型：
--
作者：
Daffern, Pamela J.;Pfeifer, Philippe H.;Ember, Julia A.;Hugli, Tony E.
强效趋化因子C5 a的炎症作用已在多种人类细胞类型上得到充分表征，包括嗜中性粒细胞、单核细胞、嗜碱性粒细胞和嗜酸性粒细胞。C3 a的细胞效应不太明确。已经发表了关于中性粒细胞C3 a活化的矛盾报告。最近的报道，C3 a激活嗜碱性粒细胞和嗜酸性粒细胞促使我们重新研究C3 a刺激对嗜酸性粒细胞的影响。我们假设，C3 a激活嗜酸性粒细胞，细胞是目前在大多数中性粒细胞的准备工作，可能会导致中性粒细胞活化。使用98%纯度的中性粒细胞，我们观察到在用C3 a、重组人C3 a（rhC 3a）或合成C3 a类似物C3 a 57-77，Y 57刺激后没有细胞活化的证据。纯化至> 98%纯度的嗜酸性粒细胞通过C3 a、rhC 3a和合成C3 a类似物刺激显示浓度依赖性极化、趋化性和酶释放。C3 a的非活性形式C3 adesArg未能刺激嗜酸性粒细胞或嗜中性粒细胞。使用含有5-9%嗜酸性粒细胞的中性粒细胞制剂，暴露于C3 a后，高达20%的中性粒细胞发生极化。同样，我们证明了C3 a刺激的嗜酸性粒细胞的上清液促进中性粒细胞的趋化性。在C5 a受体（C5 aR）抗体存在下重复嗜酸性粒细胞极化实验，以显示C3 a和C5 a与不同受体相互作用。在存在完全阻断C5 a活化的浓度的抗C5 aR抗体的情况下，C3 a活化嗜酸性粒细胞。我们的结论是，嗜酸性粒细胞直接激活C3 a或C5 a，而C3 a未能激活中性粒细胞。C3 a通过与C5 aR不同的受体作用于嗜酸性粒细胞。由于中性粒细胞是间接刺激的C3 a，嗜酸性粒细胞污染中性粒细胞的准备工作可以解释早期的报告，C3 a激活人类中性粒细胞。
Inflammatory action of the potent chemotaxin C5a has been well characterized on a variety of human cell types, including neutrophils, monocytes, basophils, and eosinophils. The cellular effects of C3a are less well defined. Contradictory reports have been published for C3a activation of neutrophils. Recent reports that C3a activates both basophils and eosinophils prompted us to reinvestigate the effects of C3a stimulation on eosinophils. We hypothesized that C3a activation of eosinophils, cells that are present in most neutrophil preparations, might lead to neutrophil activation. Using neutrophils of 98% purity, we observed no evidence of cellular activation after stimulation with either C3a, recombinant human C3a (rhC3a), or the synthetic C3a analogue C3a 57-77, Y57. Eosinophils purified to > 98% purity displayed concentration-dependent polarization, chemotaxis, and enzyme release by stimulation with C3a, rhC3a, and the synthetic C3a analogue. An inactive form of C3a, C3adesArg, failed to stimulate either eosinophils or neutrophils. Using neutrophil preparations containing 5-9% eosinophils, up to 20% of neutrophils became polarized after exposure to C3a. Likewise, we demonstrated that supernatant from C3a-stimulated eosinophils promotes neutrophil chemotaxis. Eosinophil polarization experiments were repeated in the presence of antibody to the C5a receptor (C5aR) to show that C3a and C5a interact with different receptors. C3a activates eosinophils in the presence of anti-C5aR antibody at concentrations that fully block C5a activation. We conclude that eosinophils are directly activated by either C3a or C5a, whereas C3a failed to activate neutrophils. C3a acts on eosinophils via a receptor that is distinct from C5aR. Since neutrophils are indirectly stimulated by C3a, eosinophils contaminating neutrophil preparations may explain earlier reports that C3a activates human neutrophils.
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DOI：
10.1073/pnas.87.17.6813
发表时间：
1990-09-01
影响因子：
11.1
作者：
BISCHOFF, SC;DEWECK, AL;DAHINDEN, CA
通讯作者：
DAHINDEN, CA
DOI：
10.1159/000232622
发表时间：
1980-01-01
期刊：
INTERNATIONAL ARCHIVES OF ALLERGY AND APPLIED IMMUNOLOGY
影响因子：
--
作者：
DAMERAU, B;GRUNEFELD, E;VOGT, W
通讯作者：
VOGT, W
DOI：
10.1016/0006-291x(91)91683-4
发表时间：
1991-03-29
影响因子：
3.1
作者：
FUKUOKA, Y;YASUI, A;TACHIBANA, T
通讯作者：
TACHIBANA, T
影响因子：
6.5
作者：
BRUIJNZEEL, PLB;KUIJPER, PHM;KOENDERMAN, L
通讯作者：
KOENDERMAN, L
影响因子：
5.4
作者：
GERARDYSCHAHN, R;AMBROSIUS, D;BITTERSUERMANN, D
通讯作者：
BITTERSUERMANN, D