Golenbock D T, Liu Y, Millham F H, Freeman M W, Zoeller R A
Department of Internal Medicine, Boston City Hospital, Massachusetts.
J Biol Chem. 1993 Oct 15;268(29):22055-9.
Cardiovascular collapse associated with Gram-negative septicemia is believed to result from the stimulation of phagocytes by bacterial lipopolysaccharide (endotoxin, LPS). It remains unclear how endotoxin activates phagocytes, but recent evidence suggests the involvement of the glycosyl phosphatidylinositol-linked myelocyte antigen, CD14. We report that transfection of human CD14 into Chinese hamster ovary fibroblasts transfers macrophage-like responsiveness to otherwise LPS-unresponsive cells. These data demonstrate that LPS-induced responsiveness can be transferred to a heterologous non-responder cell type by expression of a single leukocyte-specific gene product.
与革兰氏阴性败血症相关的心血管衰竭被认为是由细菌脂多糖（内毒素，LPS）刺激吞噬细胞所致。内毒素如何激活吞噬细胞尚不清楚，但最近的证据表明糖基磷脂酰肌醇连接的骨髓细胞抗原CD14参与其中。我们报告，将人CD14转染到中国仓鼠卵巢成纤维细胞中，可将巨噬细胞样反应性转移到原本对LPS无反应的细胞。这些数据表明，通过表达单一的白细胞特异性基因产物，LPS诱导的反应性可以转移到异源无反应细胞类型。
