Seljelid R, Silverstein S C, Cohn Z A
J Cell Biol. 1973 May;57(2):484-98. doi: 10.1083/jcb.57.2.484.
The effect of polycations on cultured mouse peitoneal macrophages has been examined. Polycations, at concentrations greater than 5 microg/ml, are toxic for macrophages) as measured by failure of the cells to exclude vital dyes. At toxic concentrations polycations bind in large amounts to nuclei and endoplasmic reticulum, while at nontoxic levels polycations bind selectively to the cell surface. Nontoxic concentrations of polycations stimulate binding of reovirus double-stranded (ds) RNA to the macrophages by forming polycation-dsRNA complexes either in the medium or at the cell surface. These complexes enter the cell in endocytic vacuoles and are concentrated in secondary lysosomes. Despite exposure to the acid hydrolases within this cell compartment, the dsRNA and the polycation (poly-L-lysine) are conserved in a macromolecular form within the vacuolar system. The mechanism(s) by which the uptake of infectious nucleic acids and the induction of interferon by dsRNA are stimulated by polycations are discussed.
已对聚阳离子对培养的小鼠腹腔巨噬细胞的作用进行了研究。浓度大于5微克/毫升的聚阳离子对巨噬细胞有毒性(通过细胞无法排除活性染料来衡量)。在有毒浓度下,聚阳离子大量结合到细胞核和内质网,而在无毒水平时,聚阳离子选择性地结合到细胞表面。无毒浓度的聚阳离子通过在培养基中或细胞表面形成聚阳离子 - 双链RNA复合物来刺激呼肠孤病毒双链(ds)RNA与巨噬细胞的结合。这些复合物通过内吞泡进入细胞并集中在次级溶酶体中。尽管暴露于该细胞区室内的酸性水解酶,但双链RNA和聚阳离子(聚-L-赖氨酸)以大分子形式在液泡系统中得以保留。讨论了聚阳离子刺激感染性核酸摄取和双链RNA诱导干扰素的机制。