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首页> 外文期刊>Molecular biology of the cell >Renitence vacuoles facilitate protection against phagolysosomal damage in activated macrophages
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Renitence vacuoles facilitate protection against phagolysosomal damage in activated macrophages

机译：促进液泡促进活性巨噬细胞对吞噬血糖损伤的保护

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摘要

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 phago-somes. 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.
机译：作为专业的吞噬细胞，巨噬细胞易受其摄取的病原体和有害颗粒造成的内溶血体膜损伤。巨噬细胞是否具有限制这些损坏的机制并不充分了解。以前，我们报告了一种现象，称为“诱导诱导”，其中巨噬细胞（LPS）活化受到巨噬细胞的激活，保护其尾溶胶抗二氧化硅珠粒吞噬作用引发的损伤。为了获得该过程的机械洞察，我们分析了LPS活化与休息巨噬细胞的急性和形态特征的动力学，如二氧化硅珠介导的损伤。我们发现了在二氧化硅珠吞噬作用中的LPS激活但不静息巨噬细胞中形成的新型真空结构。由于它们与迫害性和抗损害性质的相关性，我们称之为“促进液泡”（RVS）。在与膜荷丝卷曲和大磷肿瘤相关的过程中，RV与二氧化硅珠子吸收成一致。然而，与正常的宏观体（MPS）不同，其在形成20分钟内收缩，RV持续含有含珠的蜂鸣器。 RVS与溶酶体融合，而相关的吞噬物质通常没有。这些发现与其中RVS作为持久性MPS的模型一致，防止损伤吞噬物质和完整溶酶体之间的融合，从而保持内溶血剂完整性。

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