Czuprynski C J, Balish E
Infect Immun. 1981 Jul;33(1):103-8. doi: 10.1128/iai.33.1.103-108.1981.
Listeria monocytogenes induced aggregation of rat platelets in vitro and stimulated the nonlytic release of [3H]serotonin. Listeria-induced platelet aggregation and serotonin release required the presence of intact Listeria, was maximal at a 1:1 Listeria/platelet ratio, required a plasma cofactor, and was not inhibited by indomethacin, acetylsalicylic acid, or apyrase. Aggregation either of platelets in platelet-rich plasma with adenosine diphosphate or of washed platelets with thrombin resulted in the release of a listericidin from the platelets; however, direct interaction of L. monocytogenes with platelet-rich plasma did not kill Listeria. The ability of rats to clear an intravenous challenge of L. monocytogenes (0.005 50% lethal dose), as determined by the recovery of viable L. monocytogenes from the spleen and liver, was unaffected by prior treatment with antiplatelet serum.
单核细胞增生李斯特菌在体外可诱导大鼠血小板聚集,并刺激[3H]5-羟色胺的非溶解性释放。李斯特菌诱导的血小板聚集和5-羟色胺释放需要完整的李斯特菌存在,在李斯特菌与血小板比例为1:1时达到最大值,需要血浆辅助因子,且不受吲哚美辛、乙酰水杨酸或腺苷三磷酸双磷酸酶的抑制。富含血小板血浆中的血小板与二磷酸腺苷聚集,或洗涤后的血小板与凝血酶聚集,都会导致血小板释放一种杀菌素;然而,单核细胞增生李斯特菌与富含血小板血浆的直接相互作用并不会杀死李斯特菌。通过从脾脏和肝脏中回收活的单核细胞增生李斯特菌来确定,大鼠清除静脉注射的单核细胞增生李斯特菌(0.005 50%致死剂量)的能力不受抗血小板血清预处理的影响。