Goren M B, Vatter A E, Fiscus J
J Leukoc Biol. 1987 Feb;41(2):122-9. doi: 10.1002/jlb.41.2.122.
The survival of some intracellular pathogens within macrophages may be aided by an ability of the organism to antagonize, from within the entrapping phagosome, its fusion with lysosomes. On the other hand, certain polyanionic agents have been implicated in imposing a similar block to fusion from the lysosomal domain--because the transfer of various foreign markers from lysosomes to newly formed phagosomes is remarkably inhibited in these polyanion-containing cells. Based on an analysis of various observations and our own recent data, we propose that the polyanionics do not, in fact, prevent phagosome-lysosome fusion but, instead, physically entrap the usual markers in a gelatinous matrix within the lysosomes. This view accounts for many paradoxical consequences of polyanionic accumulation and for the curiously normal behavior of macrophages that are presumed to be suffering from such a crucial intracellular dysfunction.
某些细胞内病原体在巨噬细胞内的存活可能得益于该生物体从被包裹的吞噬小体内部拮抗其与溶酶体融合的能力。另一方面，某些聚阴离子试剂被认为会从溶酶体区域对融合施加类似的阻断作用——因为在这些含有聚阴离子的细胞中，各种外来标记物从溶酶体向新形成的吞噬小体的转移受到显著抑制。基于对各种观察结果和我们自己最近数据的分析，我们提出聚阴离子实际上并不会阻止吞噬小体 - 溶酶体融合，而是相反，将通常的标记物物理性地截留在溶酶体内的凝胶状基质中。这一观点解释了聚阴离子积累的许多矛盾后果，以及那些被认为患有这种关键细胞内功能障碍的巨噬细胞奇怪的正常行为。
