Department of Intensive Care Medicine, Academic Medical Center, Sanquin Research, Sanquin Blood Bank, Amsterdam, the Netherlands.
Transfus Med Hemother. 2012 Oct;39(5):353-61. doi: 10.1159/000342229. Epub 2012 Sep 6.
Anemia is a frequently encountered problem in the critically ill patient. The inability to compensate for anemia includes several mechanisms, collectively referred to as anemia of inflammation: reduced production of erythropoietin, impaired bone marrow response to erythropoietin, reduced iron availability, and increased red blood cell (RBC) clearance. This review focuses on mechanisms of RBC clearance during inflammation. We state that phosphatidylserine (PS) expression in inflammation is mainly enhanced due to an increase in ceramide, caused by an increase in sphingomyelinase activity due to either platelet activating factor, tumor necrosis factor-α, or direct production by bacteria. Phagocytosis of RBCs during inflammation is mediated via RBC membrane protein band 3. Reduced deformability of RBCs seems an important feature in inflammation, also mediated by band 3 as well as by nitric oxide, reactive oxygen species, and sialic acid residues. Also, adherence of RBCs to the endothelium is increased during inflammation, most likely due to increased expression of endothelial adhesion molecules as well as PS on the RBC membrane, in combination with decreased capillary blood flow. Thereby, clearance of RBCs during inflammation shows similarities to clearance of senescent RBCs, but also has distinct entities, including increased adhesion to the endothelium.
贫血是危重病患者中经常遇到的问题。无法代偿贫血包括几种机制，统称为炎症性贫血：促红细胞生成素生成减少、骨髓对促红细胞生成素反应受损、铁供应减少和红细胞 (RBC) 清除增加。本综述重点介绍炎症期间 RBC 清除的机制。我们指出，炎症中 PS 的表达主要是由于神经酰胺增加所致，这是由于血小板激活因子、肿瘤坏死因子-α 或细菌直接产生导致鞘磷脂酶活性增加所致。炎症期间 RBC 的吞噬作用是通过 RBC 膜蛋白带 3 介导的。RBC 的变形能力降低似乎是炎症的一个重要特征，这也通过带 3 以及一氧化氮、活性氧和唾液酸残基介导。此外，炎症期间 RBC 与内皮细胞的黏附增加，这很可能是由于内皮细胞黏附分子以及 RBC 膜上 PS 的表达增加，同时毛细血管血流减少所致。因此，炎症期间 RBC 的清除与衰老 RBC 的清除具有相似性，但也有明显的不同，包括与内皮的黏附增加。
