...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Inhibition of chemotaxis of neutrophil leukocytes to interleukin-8 by endotoxins of various bacteria.
【24h】

Inhibition of chemotaxis of neutrophil leukocytes to interleukin-8 by endotoxins of various bacteria.

机译：各种细菌的内毒素抑制嗜中性白细胞对白细胞介素8的趋化性。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The effects of endotoxins from various bacteria (Escherichia coli, Klebsiella pneumoniae, Vibrio cholerae, Shigella flexneri, Salmonella typhosa, and Pseudomonas aeruginosa) on chemotaxis of neutrophil leukocytes to formyl peptide and interleukin-8 were tested in an improved chemotaxis assay involving a "sparse-pore" polycarbonate (Nuclepore) membrane in a Boyden-type chamber. The possible chemotactic activity of the endotoxins themselves were tested by the same technique. In addition, the effects of these substances on random motility of neutrophils were tested with a corresponding assay involving similar chambers fitted with membranes of standard pore density. Possible activation of the complement system of serum by each endotoxin was tested with sheep erythrocyte assays and the maximum endotoxin concentration (100 micrograms/ml) used in the chemotaxis and motility assays. All endotoxins inhibited chemotaxis of neutrophils to interleukin-8. No endotoxin affected chemotaxis to formyl peptide or was itself chemotactic for neutrophils. Endotoxin of S. flexneri inhibited random motility of neutrophils, while the others had no such effect. Endotoxins of K. pneumoniae and of P. aeruginosa produced moderate and marked inhibition, respectively, of total complement, as measured by hemolysis of sheep erythrocytes, without affecting the levels of C3c and C4 in these assays. Endotoxins of the other bacteria had no demonstrable effect in any of these assays of complement activation. These results suggest that chemotaxis to interleukin-8 may be mediated by cellular mechanisms different from those involved in chemotaxis to formyl peptide. Furthermore, the presence of these endotoxins could be significant for the suppression of neutrophil accumulation in inflammatory lesions mediated by interleukin-8.
机译：在改良的趋化性试验中，测试了来自各种细菌（大肠杆菌，肺炎克雷伯菌，霍乱弧菌，弗氏志贺氏菌，鼠伤寒沙门氏菌和铜绿假单胞菌）内毒素对嗜中性白细胞对甲酰肽和白介素8趋化性的影响。博登型腔室中的“多孔”聚碳酸酯（Nuclepore）膜。内毒素本身可能的趋化活性用相同的技术测试。另外，这些物质对嗜中性粒细胞随机运动的影响用相应的试验进行了测试，该试验涉及装有标准孔密度膜的类似室。用绵羊红细胞测定法测试了每种内毒素对血清补体系统的可能激活作用，并在趋化性和运动性测定法中使用了最大内毒素浓度（100微克/毫升）。所有内毒素均抑制中性粒细胞对白介素8的趋化性。没有内毒素影响对甲酰肽的趋化性，或本身对中性粒细胞的趋化性。弗氏链球菌的内毒素抑制中性粒细胞的随机运动，而其他的则没有这种作用。通过羊红细胞的溶血测定，肺炎克雷伯菌和铜绿假单胞菌的内毒素分别产生总补体的中度和显着抑制，而在这些测定中不影响C3c和C4的水平。在所有这些补体激活试验中，其他细菌的内毒素均无明显作用。这些结果表明对白细胞介素8的趋化性可能是由不同于对甲酰肽的趋化性的细胞机制介导的。此外，这些内毒素的存在对于抑制由白介素8介导的炎性病变中的中性粒细胞积累可能是重要的。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号