MECHANISMS OF BIOMATERIAL-INDUCED SUPEROXIDE RELEASE BY NEUTROPHILS

MECHANISMS OF BIOMATERIAL-INDUCED SUPEROXIDE RELEASE BY NEUTROPHILS
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DOI:
10.1002/jbm.820280313
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发表时间:
1994-03-01
期刊:
JOURNAL OF BIOMEDICAL MATERIALS RESEARCH
影响因子:
--
通讯作者:
SIMMONS, RL
SIMMONS, RL
中科院分区:
其他
文献类型:
--
作者:
KAPLAN, SS;BASFORD, RE;SIMMONS, RL

文献摘要

被引文献

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以生物材料为中心的感染是导致假体和器官失败的重要原因。由于中性粒细胞介导了宿主对感染的防御,因此利用外科常用的三种材料研究了生物材料对中性粒细胞超氧化物歧化释放的影响及其机制。接枝材料为膨体聚四氟乙烯(PTFE)、聚氨酯和机织涤纶。聚苯乙烯,一种常用的实验室支持容器也被研究。聚苯乙烯和聚氨酯都被激活,但血清是可抑制的,而聚四氟乙烯是不激活的,机织涤纶不是激活的,除非血清存在。这些材料使用的信号机制表现出时间和材料的依赖性。百日咳毒素抑制G蛋白依赖的激活对生物材料诱导的激活作用很小或没有影响,而FMLP诱导的生物材料相关细胞的激活被抑制。用星形孢子素抑制蛋白激酶C可显著抑制聚苯乙烯诱导的活化,但对聚氨酯的抑制作用不明显,而对含血清的机织涤纶的激活作用更小。这些研究表明,生物材料接触诱导的中性粒细胞激活不同于悬浮液中细胞的激活,并表明一种材料上的激活机制不能外推到其他材料上的机制。(C)1994年John Wiley父子公司。
Biomaterial-centered infection is an important cause of the failure of prosthetic implants and organs. Because neutrophils mediate host defense against infection, the effect of biomaterials on neutrophil superoxide release and the mechanism of that effect were investigated using three materials commonly employed in surgical practice. The graft materials were expanded polytetrafluorethylene (PTFE), polyurethane and woven dacron. Polystyrene, a commonly used laboratory support vessel, was also studied. Both polystyrene and polyurethane were activating, but serum inhibitable, whereas PTFE was nonactivating, and woven dacron was not activating unless serum was present. The signaling mechanisms used by these materials demonstrated time and material dependency. Pertussis toxin inhibition of G protein-dependent activation had little or no effect on biomaterial induced activation, whereas FMLP-induced activation of the same biomaterial-associated cells was inhibited. Protein kinase C inhibition with staurosporine greatly inhibited polystyrene-induced activation, but had only a partial effect with polyurethane and even less effect with the activation associated with serum-treated woven dacron. These studies demonstrated that biomaterial contact-induced neutrophil activation differed from that described for cells in suspension, and showed that activation mechanisms on one material cannot be extrapolated to mechanisms on other materials. (C) 1994 John Wiley and Sons, Inc.