Purified human basophils do not generate LTB4.

Purified human basophils do not generate LTB4.
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纯化的人嗜碱性粒细胞不会产生 LTB4。

DOI:
10.1016/0006-2952(87)90632-0
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发表时间:
1987
影响因子:
5.8
通讯作者:
Peters,SP
Peters,SP
中科院分区:
医学2区
文献类型:
--
作者:
Warner,JA;Freeland,HS;MacGlashanJr,DW;Lichtenstein,LM;Peters,SP

文献摘要

被引文献

相似文献

我们研究了花生四烯酸(AA)的5-脂氧合酶衍生物在纯化的人嗜碱性细胞中的释放,并将其与在人肺肥大细胞中获得的类似结果进行了比较。我们发现纯化的嗜碱性细胞(平均纯度为51±6%)用0.1 μg/ml抗ige释放的组胺(35±9%)和ltc4(32±10 ng/10 6个细胞)攻击,但不能释放可测量的免疫反应性ltb4。相反,非特异性刺激A23187引起组胺和ltc4(279±95 ng/ 10.6个细胞)和ltb4(148±41 ng/ 10.6个细胞)的释放。对数据的进一步分析显示,LTB - 4的释放水平与嗜碱性粒细胞的纯度呈反比关系,这强烈表明污染的单核细胞负责LTB - 4的合成。纯化的人肺肥大细胞已被证明释放6ng的免疫反应性ltb4106细胞,这表明嗜碱性细胞在ige介导的攻击后释放的ltb4显著减少。在一系列用[3h] AA预标记的高纯度嗜碱性粒细胞的实验中,我们证明暴露于0.1 μg/ml抗ige导致[3h] ltc4释放,但未检测到[3h] lt4,而暴露于1.0 μg/ml A23187导致[3h] ltc4释放,少量的[3h] LTB 4、[3h] lt4和[3h] lt4释放。用抗ige或A23187攻击后,我们在细胞颗粒中未检测到任何[3h] LTB - 4,这表明LTB - 4没有合成并保留在细胞颗粒中。最后,我们发现外源添加的[3h] ltb4无论是单独被嗜碱性细胞代谢,还是被抗ige (O. 1 μg/ml)刺激的嗜碱性细胞代谢。
We investigated the release of the 5-lipoxygenase derivatives of arachidonic acid (AA) in purified human basophils and compared them with similar results obtained in the human lung mast cell. We have shown that purified basophils (average purity= 51±6%) challenged with 0.1 μg/ml anti-IgE released histamine (35±9%), and LTC 4 (32±10 ng/10 6 cells) but failed to release measurable quantities of immunoreactive LTB 4. In contrast, the non-specific stimulus, A23187, caused the release of histamine and both LTC 4 (279±95 ng/10 6 cells) and LTB 4 (148±41 ng/10 6 cells). Closer analysis of the data revealed an inverse relationship between the levels of LTB 4 released and the purity of the basophils, strongly suggesting that the contaminating monocytes were responsible for LTB 4 synthesis. Purified human lung mast cells have been shown to release 6 ng of immunoreactive LTB 4 10 6 cells, indicating that basophils release significantly less LTB 4 following an IgE-mediated challenge. In a series of experiments using highly purified basophils prelabeled with [3 H] AA, we demonstrated that exposure to 0.1 μg/ml anti-IgE led to the release of [3 H] LTC 4, with no detectable [3 H] LTB 4, whereas exposure to 1.0 μg/ml A23187 caused the release of [3 H] LTC 4 and smaller quantities of [3 H] LTB 4,[3 H] LTD 4, and [3 H] LTE 4. We failed to detect any [3 H] LTB 4 in the cell pellet following challenge with either anti-IgE or A23187, indicating that LTB 4 was not synthesized and retained within the cell pellet. Finally, we found that exogenously added [3 H] LTB 4 was not metabolized, either by basophils alone or by basophils stimulated with anti-IgE (O. 1 μg/ml).