Boggs D R, Marsh J C, Chervenick P A, Bishop C R, Cartwright G E, Wintrobe M M
J Exp Med. 1967 Nov 1;126(5):851-70. doi: 10.1084/jem.126.5.851.
Normal dog plasma and serum, human, rat, and Swiss-Webster mouse plasma, phytohemagglutinin, sheep red cells, mumps and influenza vaccine, fibrinogen, and endotoxin injected before irradiation led to an increased number of endogenously derived spleen colonies in irradiated mice. Spleen weight and uptake of radioactive iron and iododeoxyuridine into such spleens were also increased. The relationship between these parameters of splenic hematopoiesis was unchanged by plasma injection suggesting that, while the number of colonies was increased, the composition of individual colonies was unchanged. This conclusion was supported by studies on plethoric mice in which splenic erythropoiesis is abolished. Increased splenic hematopoiesis was accompanied by an increase in the volume of packed red blood cells 10 days after irradiation. The total volume of plasma injected, the number of days of plasma injection preceding irradiation, and the route of administration were all important variables influencing the effect of plasma injections. Crude fractions of human albumin and gamma globulin, cortisol, C57BL (maternal) and DBA (paternal) mouse plasma, and isogeneic plasma were without effect. The ineffectiveness of isogeneic and closely related allogeneic plasma rendered unlikely the hypothesis that this effect represented the presence of homeostatic hematopoietic regulating factors in plasma. The increased hematopoiesis induced with plasma appeared to be limited to the spleen, for increased bone marrow hematopoiesis was not detected. Certain observations suggested that the effect of plasma may not be due to an antigenic or an inflammatory effect. From current observations, it was unclear whether the increased colonies induced by plasma were representative of expansion of the colony-forming cell pool or of increased efficiency of growth of the fraction surviving irradiation.
正常犬血浆和血清、人、大鼠及瑞士-韦伯斯特小鼠血浆、植物血凝素、绵羊红细胞、腮腺炎和流感疫苗、纤维蛋白原以及在照射前注射的内毒素,均可使受照射小鼠内源性脾集落数量增加。脾脏重量以及放射性铁和碘脱氧尿苷在这些脾脏中的摄取量也会增加。血浆注射并未改变脾造血这些参数之间的关系,这表明虽然集落数量增加了,但单个集落的组成并未改变。对脾性多血质小鼠的研究支持了这一结论,在这类小鼠中脾红细胞生成被消除。照射后10天,脾造血增加伴随着红细胞压积体积的增加。注射血浆的总体积、照射前注射血浆的天数以及给药途径都是影响血浆注射效果的重要变量。人白蛋白和γ球蛋白的粗提物、皮质醇、C57BL(母本)和DBA(父本)小鼠血浆以及同基因血浆均无作用。同基因和密切相关的异基因血浆无作用,这使得这种效应代表血浆中存在稳态造血调节因子这一假设不太可能成立。血浆诱导的造血增加似乎仅限于脾脏,因为未检测到骨髓造血增加。某些观察结果表明,血浆的作用可能不是由于抗原或炎症效应。从目前的观察来看,尚不清楚血浆诱导的集落增加是代表集落形成细胞池的扩大还是代表照射后存活部分生长效率的提高。