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重组人白细胞介素-1β使人类多形核白细胞对刺激诱导的髓过氧化物酶释放产生预刺激作用。

Recombinant human interleukin-1 beta primes human polymorphonuclear leukocytes for stimulus-induced myeloperoxidase release.

作者信息

Dularay B, Elson C J, Clements-Jewery S, Damais C, Lando D

机构信息

Medical School, University of Bristol, England.

出版信息

J Leukoc Biol. 1990 Feb;47(2):158-63. doi: 10.1002/jlb.47.2.158.

DOI:10.1002/jlb.47.2.158
PMID:2154524
Abstract

Recombinant human Interleukin-1 (rhIL-1) beta was found to enhance stimulus-induced granule exocytosis from human polymorphonuclear leukocytes (PMNs). PMNs were incubated with rhIL-1 beta and then stimulated with either heat-aggregated IgG (Hagg) or N-formyl-methionyl leucylphenylalanine (FMLP). The release of the azurophil enzyme myeloperoxidase (MPO) was measured. Low concentrations of stimuli (10 micrograms/ml Hagg, 2.5 X 10(-9) M FMLP) did not stimulate degranulation in the absence of rhIL-1 beta. However, such concentrations elicited marked degranulation from PMNs preincubated with rhIL-1 beta (0.2-100 ng/ml). The enhancement of degranulation was dependent on the concentration of rhIL-1 beta employed and on the period of incubation. In other experiments, the effect of rhIL-1 beta on the PMN oxidative response was determined. rhIL-1 beta did not directly stimulate the production of superoxide anions or enhance the oxidative response to Hagg or FMLP. It is suggested that in rheumatoid joints, IL-1 beta may potentiate PMN degranulation, but not their oxidative response.

摘要

已发现重组人白细胞介素-1(rhIL-1)β可增强人多形核白细胞(PMN)刺激诱导的颗粒胞吐作用。将PMN与rhIL-1β孵育,然后用热聚集IgG(Hagg)或N-甲酰甲硫氨酰亮氨酰苯丙氨酸(FMLP)刺激。测量嗜天青酶髓过氧化物酶(MPO)的释放。在没有rhIL-1β的情况下,低浓度刺激物(10微克/毫升Hagg,2.5×10^(-9) M FMLP)不会刺激脱颗粒。然而,这些浓度可引起与rhIL-1β(0.2 - 100纳克/毫升)预孵育的PMN显著脱颗粒。脱颗粒的增强取决于所用rhIL-1β的浓度和孵育时间。在其他实验中,确定了rhIL-1β对PMN氧化反应的影响。rhIL-1β不会直接刺激超氧阴离子的产生,也不会增强对Hagg或FMLP的氧化反应。提示在类风湿关节中,IL-1β可能增强PMN脱颗粒,但不会增强其氧化反应。

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