Suppr超能文献

人热休克蛋白60和70对内毒素诱导的炎症的多种调节活性。

Diverse regulatory activity of human heat shock proteins 60 and 70 on endotoxin-induced inflammation.

作者信息

Bangen Jörg M, Schade F Ulrich, Flohé Stefanie B

机构信息

Surgical Research, Department of Trauma Surgery, University Hospital Essen, University Duisburg-Essen, Virchowstr. 171, D-45147 Essen, Germany.

出版信息

Biochem Biophys Res Commun. 2007 Aug 3;359(3):709-15. doi: 10.1016/j.bbrc.2007.05.167. Epub 2007 May 30.

Abstract

Tissue injury is often associated with bacterial infection. Intracellular heat shock proteins (HSPs) are released from damaged tissue, come in contact with cells of the immune system, and might affect the immune response against bacteria. In the present study, we investigated the capacity of highly purified human HSP60 and HSP70 to modulate the response of human peripheral blood-derived mononuclear cells (PBMC) to lipopolysaccharide (LPS). HSP70 but not HSP60 decreased the LPS-induced secretion of TNF-alpha when added simultaneously with LPS. In contrast, HSP60 and HSP70 primed PBMC for enhanced secretion of TNF-alpha when added 24h prior to the stimulation with LPS. Neither HSP60 nor HSP70 alone induced the release of TNF-alpha. The capacity of LPS to bind to monocytes was not affected by HSPs, but HSP70 increased the expression of Toll-like receptor 4. Thus, HSP60 and HSP70 released upon tissue damage might play a role in the regulation of bacteria-induced inflammation.

摘要

组织损伤常与细菌感染相关。细胞内热休克蛋白(HSPs)从受损组织中释放出来,与免疫系统细胞接触,并可能影响针对细菌的免疫反应。在本研究中,我们研究了高度纯化的人HSP60和HSP70调节人外周血来源单核细胞(PBMC)对脂多糖(LPS)反应的能力。当与LPS同时添加时,HSP70而非HSP60降低了LPS诱导的TNF-α分泌。相反,当在LPS刺激前24小时添加时,HSP60和HSP70使PBMC对TNF-α的分泌增强。单独的HSP60和HSP70均未诱导TNF-α的释放。HSPs不影响LPS与单核细胞的结合,但HSP70增加了Toll样受体4的表达。因此,组织损伤时释放的HSP60和HSP70可能在细菌诱导的炎症调节中起作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验