Lin Tian, Liu Jialin, Huang Feng, Engelen Tjitske Sr van, Thundivalappil Sujatha R, Riley Frank E, Super Michael, Watters Alexander L, Smith Ann, Brinkman Nathan, Ingber Donald E, Warren H Shaw
Department of Pediatrics, Infectious Disease Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, United States of America.
Department of Pediatrics, Infectious Disease Unit, Massachusetts General Hospital, Boston, Massachusetts, United States of America.
Mol Med. 2016 Sep;22:22-31. doi: 10.2119/molmed.2016.00006. Epub 2016 Jan 8.
Infusion of the heme-binding protein hemopexin has been proposed as a novel approach to decrease heme-induced inflammation in settings of red blood cell breakdown, but questions have been raised as to possible side effects related to protease activity and inhibition of chemotaxis. We evaluated protease activity and effects on chemotaxis of purified plasma hemopexin obtained from multiple sources as well as a novel recombinant fusion protein Fc-hemopexin. Amidolytic assay was performed to measure the protease activity of several plasma-derived hemopexin and recombinant Fc-hemopexin. Hemopexin was added to the human monocyte culture in the presence of lipopolysaccharides (LPS), and also injected into mice intravenously (i.v.) 30 min before inducing neutrophil migration via intraperitoneal (i.p.) injection of thioglycolate. Control groups received the same amount of albumin. Protease activity varied widely between hemopexins. Recombinant Fc-hemopexin bound heme, inhibited the synergy of heme with LPS on tumor necrosis factor (TNF) production from monocytes, and had minor but detectable protease activity. There was no effect of any hemopexin preparation on chemotaxis, and purified hemopexin did not alter the migration of neutrophils into the peritoneal cavity of mice. Heme and LPS synergistically induced the release of LTB4 from human monocytes, and hemopexin blocked this release, as well as chemotaxis of neutrophils in response to activated monocyte supernatants. These results suggest that hemopexin does not directly affect chemotaxis through protease activity, but may decrease heme-driven chemotaxis and secondary inflammation by attenuating the induction of chemoattractants from monocytes. This property could be beneficial in some settings to control potentially damaging inflammation induced by heme.
输注血红素结合蛋白血红素结合珠蛋白已被提议作为一种新方法,用于在红细胞分解的情况下减少血红素诱导的炎症,但有人对与蛋白酶活性和趋化性抑制相关的可能副作用提出了疑问。我们评估了从多个来源获得的纯化血浆血红素结合珠蛋白以及新型重组融合蛋白Fc-血红素结合珠蛋白的蛋白酶活性及其对趋化性的影响。进行酰胺水解测定以测量几种血浆来源的血红素结合珠蛋白和重组Fc-血红素结合珠蛋白的蛋白酶活性。在存在脂多糖(LPS)的情况下,将血红素结合珠蛋白添加到人单核细胞培养物中,并在通过腹腔内(i.p.)注射巯基乙酸盐诱导中性粒细胞迁移前30分钟静脉内(i.v.)注射到小鼠体内。对照组接受相同量的白蛋白。不同来源的血红素结合珠蛋白之间的蛋白酶活性差异很大。重组Fc-血红素结合珠蛋白结合血红素,抑制血红素与LPS对单核细胞肿瘤坏死因子(TNF)产生的协同作用,并且具有轻微但可检测到的蛋白酶活性。任何血红素结合珠蛋白制剂对趋化性均无影响,纯化的血红素结合珠蛋白也未改变中性粒细胞向小鼠腹腔的迁移。血红素和LPS协同诱导人单核细胞释放白三烯B4(LTB4),血红素结合珠蛋白可阻断这种释放以及中性粒细胞对活化单核细胞上清液的趋化性。这些结果表明,血红素结合珠蛋白不会通过蛋白酶活性直接影响趋化性,但可能通过减弱单核细胞趋化因子的诱导来降低血红素驱动的趋化性和继发性炎症。在某些情况下,这种特性可能有助于控制由血红素诱导的潜在破坏性炎症。