Wolf J E, Massof S E, Sherwin J R, Considine R V
Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.
Infect Immun. 1992 Jul;60(7):2683-7. doi: 10.1128/iai.60.7.2683-2687.1992.
Ingestion of Histoplasma capsulatum yeast cells inhibits the oxidative burst response of murine macrophages (M phi's). Since protein kinase C (PKC) is believed to be an integral part of the signal transduction pathway involved in the production of reactive oxygen intermediates, we investigated the relationship between PKC activity and oxidative burst inhibition in H. capsulatum-containing murine peritoneal M phi's. An inhibitory effect on both basal and phorbol myristate acetate-mobilized membrane PKC activities was observed in M phi's which had ingested H. capsulatum but not latex spheres. These results suggest that one way in which H. capsulatum may disrupt the oxidative burst is through a PCK-dependent mechanism.
摄入荚膜组织胞浆菌酵母细胞会抑制小鼠巨噬细胞(M phi's)的氧化爆发反应。由于蛋白激酶C(PKC)被认为是参与活性氧中间体产生的信号转导途径的一个组成部分,我们研究了含荚膜组织胞浆菌的小鼠腹腔M phi's中PKC活性与氧化爆发抑制之间的关系。在摄入荚膜组织胞浆菌而非乳胶球的M phi's中,观察到对基础和佛波酯肉豆蔻酸酯动员的膜PKC活性均有抑制作用。这些结果表明,荚膜组织胞浆菌破坏氧化爆发的一种方式可能是通过一种依赖PKC的机制。