Paralysis of phagocyte migration due to an artificial blood substitute.

Paralysis of phagocyte migration due to an artificial blood substitute.
复制标题

人工血液替代品导致吞噬细胞迁移瘫痪。

DOI:
--
复制
发表时间:
1984
期刊:
影响因子:
20.3
通讯作者:
G. Lamkin
G. Lamkin
中科院分区:
医学1区
文献类型:
--
作者:
T. Lane;G. Lamkin

文献摘要

参考文献

被引文献

相似文献

我们研究了候选人工血液替代品Fluosol-DA(FDA)在无血清培养基中对人中性粒细胞功能的影响。在50%(vol/vol)与多形核细胞(PMN)的混合物中,FDA对PMN活力、吞噬作用、超氧阴离子生成、脱粒或杀菌活性无影响。与此形成鲜明对比的是,中性粒细胞对f-Met-Leu-Phe(fMLP)和活化血清的随机迁移和趋化作用分别被抑制98% +/-2%、95% +/-2%和88% +/-6%。FDA对趋化性的抑制不需要预孵育,具有剂量依赖性(与FDA的14% vol/vol混合物的50%抑制[ID 50]),并且在孵育1小时后通过洗涤不含FDA的PMN完全可逆,但在孵育18小时后不可逆(32% +/- 11%趋化性抑制)。FDA本身不具有趋化性,并且不损害fMLP与PMN的趋化活性或结合。FDA还抑制PMN粘附(ID 50,9 +/- 1 vol/vol%)。发现FDA的抑制组分是其清洁剂添加剂Pluronic F-68,其抑制随机迁移、趋化性和粘附,ID 50分别为1.4、2.4和2.9 mg/mL(分别相当于FDA浓度5、9和11 vol/vol%)。FDA的所有其他组分均无抑制作用。注射8 mL/kg FDA的人血浆样品和注射16 mL/kg FDA或等效浓度Pluronic F-68的兔血浆样品与自体PMN混合时,也严重抑制PMN趋化性。我们的结论是,暴露于临床相关浓度的FDA抑制PMN迁移,可能是由于抑制粘附。抑制作用完全是由于清洁剂普朗尼克F-68。含有Pluronic F-68的人工血液替代品可能会损害PMN预防或有效控制微生物感染的能力。
We investigated the effect of a candidate artificial blood substitute, Fluosol-DA (FDA), on human neutrophil function in a serum-free medium. In a 50% (vol/vol) mixture with polymorphonuclear cells (PMN), FDA had no effect on PMN viability, phagocytosis, superoxide anion generation, degranulation, or bactericidal activity. In striking contrast, the random migration and chemotaxis of PMN to both f-Met-Leu-Phe (fMLP) and activated serum were inhibited by 98% +/- 2%, 95% +/- 2%, and 88% +/- 6%, respectively. Inhibition of chemotaxis by FDA required no preincubation, was dose-dependent (50% inhibition [ID50] with a 14% vol/vol mixture with FDA), and was fully reversible by washing PMN free of FDA after one hour but not after 18 hours of incubation (32% +/- 11% inhibition of chemotaxis). FDA itself was not chemotactic and did not impair either the chemotactic activity or binding of fMLP to PMN. FDA also inhibited PMN adhesion (ID50, 9 +/- 1 vol/vol%). The inhibitory component of FDA was found to be its detergent additive, Pluronic F-68, which inhibited random migration, chemotaxis, and adhesion with ID50s of 1.4, 2.4, and 2.9 mg/mL, respectively (equivalent to FDA concentrations of 5, 9, and 11 vol/vol%, respectively). All the other components of FDA were noninhibitory. Plasma samples from humans injected with 8 mL/kg FDA and plasma samples from rabbits injected with 16 mL/kg FDA or an equivalent concentration of Pluronic F-68, when mixed with autologous PMN, also severely inhibited PMN chemotaxis. We conclude that exposure of PMN to clinically relevant concentrations of FDA inhibits PMN migration, presumably due to inhibition of adhesion. The inhibitory effect is entirely due to the detergent, Pluronic F-68. Artificial blood substitutes containing Pluronic F-68 may compromise the ability of PMN to prevent or effectively control microbial infections.
全氟化碳增强异源红细胞存活:网状内皮阻滞效应?
DOI: 10.1159/000233279
发表时间: 1983
期刊: International archives of allergy and applied immunology
影响因子: --
作者:
Castro,O;Reindorf,CA;Socha,WW;Rowe,AW
通讯作者: Rowe,AW