Immunology Graduate Program, University of Michigan Medical School, Ann Arbor, MI 48109.
Medical Scientist Training Program, University of Michigan Medical School, Ann Arbor, MI 48109.
Mol Biol Cell. 2018 Mar 1;29(5):657-668. doi: 10.1091/mbc.E17-07-0486. Epub 2017 Dec 27.
As professional phagocytes, macrophages are susceptible to endolysosomal membrane damage inflicted by the pathogens and noxious particles they ingest. Whether macrophages have mechanisms for limiting such damage is not well understood. Previously, we reported a phenomenon, termed "inducible renitence," in which lipopolysaccharide (LPS) activation of macrophages protected their endolysosomes against damage initiated by the phagocytosis of silica beads. To gain mechanistic insight into the process, we analyzed the kinetics of renitence and morphological features of LPS-activated versus resting macrophages following silica bead-mediated injury. We discovered novel vacuolar structures that form in LPS-activated but not resting macrophages following silica bead phagocytosis. Because of their correlation with renitence and damage-resistant nature, we termed these structures "renitence vacuoles" (RVs). RVs formed coincident with silica bead uptake in a process associated with membrane ruffling and macropinocytosis. However, unlike normal macropinosomes (MPs), which shrink within 20 min of formation, RVs persisted around bead-containing phagosomes. RVs fused with lysosomes, whereas associated phagosomes typically did not. These findings are consistent with a model in which RVs, as persistent MPs, prevent fusion between damaged phagosomes and intact lysosomes and thereby preserve endolysosomal integrity.
作为专业的吞噬细胞,巨噬细胞容易受到其内吞的病原体和有害物质对内溶酶体膜的损伤。目前尚不清楚巨噬细胞是否具有限制这种损伤的机制。先前,我们报道了一种现象,称为“诱导性抗性”,即脂多糖(LPS)激活巨噬细胞可保护其内溶酶体免受吞噬二氧化硅珠引发的损伤。为了深入了解这一过程的机制,我们分析了诱导性抗性的动力学以及在二氧化硅珠介导的损伤后 LPS 激活和静止巨噬细胞的形态特征。我们发现了一种新型的空泡结构,该结构仅在 LPS 激活但未静止的巨噬细胞中形成,这些结构是在吞噬二氧化硅珠后形成的。由于它们与抗性和耐损伤的性质相关,我们将这些结构称为“抗性空泡”(RV)。RV 的形成与膜皱襞和巨胞饮作用相关,与二氧化硅珠的摄取同时发生。然而,与形成后 20 分钟内收缩的正常巨胞饮体(MP)不同,RV 存在于含珠的吞噬体周围。RV 与溶酶体融合,而相关的吞噬体通常不融合。这些发现与以下模型一致,即 RV 作为持久的 MPs,可防止受损的吞噬体与完整的溶酶体融合,从而维持内溶酶体的完整性。