Effects of a chemotactic factor, N-formylmethionyl peptide, on adherence, superoxide anion generation, phagocytosis, and microtubule assembly of human polymorphonuclear leukocytes.

Effects of a chemotactic factor, N-formylmethionyl peptide, on adherence, superoxide anion generation, phagocytosis, and microtubule assembly of human polymorphonuclear leukocytes.
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趋化因子 N-甲酰甲硫氨酰肽对人多形核白细胞粘附、超氧阴离子生成、吞噬作用和微管组装的影响。

DOI:
10.5555/uri:pii:0022214379900386
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发表时间:
1979
期刊:
The Journal of laboratory and clinical medicine
影响因子:
--
通讯作者:
R. Baehner
R. Baehner
中科院分区:
--
文献类型:
--
作者:
L. Boxer;M. Yoder;S. Bonsib;M. Schmidt;P. Ho;R. Jersild;R. Baehner

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在对细胞趋化的浓度下,FMLP促进了PMN中微管的组装。当浓度高于趋化所需浓度时,FMLP可增强中性粒细胞与尼龙玻璃纤维的粘附性。用秋水仙碱可抑制PMN的黏附,但在FMLP作用下,PMN的黏附可恢复。FMLP对PMN黏附的影响是暂时的,到5min时不再明显。浓度与依从性研究中使用的浓度相似。FMLP诱导细胞短暂地产生O-2,因为在5分钟时,铁细胞色素C的还原不再明显。用细胞松弛素B预处理PMN可促进FMLP作用下PMN释放O-2。另一方面,FMLP对C3包被颗粒的吞噬功能没有影响。这些结果表明,FMLP诱导反应细胞形成一种高度黏附的质膜,这种细胞膜在很大程度上不依赖于微管的控制。由于细菌中形成了类似于AMLP的寡肽,N-甲酰化肽的作用很可能在调节炎症反应中起着重要作用。
FMLP promoted microtubule assembly in PMNs at concentrations which were chemotactic for the cells. At higher concentrations than those required for chemotaxis, FMLP enhanced the adherence of PMNs to nylon glass fibers. With colchicine, PMN adherence was inhibited, but upon exposure to FMLP, PMN adherence could be restored. The effect of FMLP on PMN adherence was transitory and was no longer evident by 5 min. At concentrations similar to those employed in the adherence studies. FMLP induced the cells to briefly generate O-2, since ferricytochrome C reduction was no longer evident by 5 min. Pretreatment of the PMNs with cytochalasin B enhanced the release of O-2 by PMNs exposed to FMLP. On the other hand, there was no effect of FMLP on phagocytosis of C3-coated particles. These results suggest that FMLP induces responsive cells to develop a hyperadherent plasma membrane which is largely independent on microtubule control. Since oligopeptides similar of AMLP are formed in bacteria, it is likely that the action of N-formylated peptides is important in regulating the inflammatory response.