Erratum: Red Blood Cell Clearance in Inflammation

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 factorα, 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.

贫血是重症患者中常见的临床问题。机体对贫血的代偿能力丧失涉及多种机制，这些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的反应受损、铁可利用度降低，以及红细胞(red blood cell, RBC)清除率升高。本综述聚焦炎症状态下的红细胞清除机制。本文指出，炎症状态下磷脂酰丝氨酸(phosphatidylserine, PS)的表达主要因神经酰胺水平升高而上调，而神经酰胺升高则源于血小板活化因子、肿瘤坏死因子α介导的鞘磷脂酶活性增强，或是细菌直接产生鞘磷脂酶。炎症状态下红细胞的吞噬作用通过红细胞膜蛋白带3(band 3)介导。红细胞变形能力降低似乎是炎症状态下的重要特征，该过程同样由带3蛋白、一氧化氮(nitric oxide, NO)、活性氧(reactive oxygen species, ROS)以及唾液酸残基介导。此外，炎症状态下红细胞与内皮细胞的黏附能力增强，这极有可能源于红细胞膜上内皮黏附分子及磷脂酰丝氨酸表达上调，同时伴随毛细血管血流量降低。综上，炎症状态下的红细胞清除过程与衰老红细胞的清除存在相似之处，但也存在包括红细胞与内皮细胞黏附增强在内的独特特征。