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首页> 外文期刊>Infection and immunity >Neisseria gonorrhoeae Porin P1.B Induces Endosome Exocytosis and a Redistribution of Lamp1 to the Plasma Membrane
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Neisseria gonorrhoeae Porin P1.B Induces Endosome Exocytosis and a Redistribution of Lamp1 to the Plasma Membrane

机译：淋病奈瑟氏球菌P1.B诱导内体胞吐和Lamp1向血浆膜的重新分布。

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The immunoglobulin A (IgA) protease secreted by pathogenic Neisseria spp. cleaves Lamp1, thereby altering lysosomes in a cell and promoting bacterial intracellular survival. We sought to determine how the IgA protease gains access to cellular Lamp1 in order to better understand the role of this cleavage event in bacterial infection. In a previous report, we demonstrated that the pilus-induced Ca2+ transient triggers lysosome exocytosis in human epithelial cells. This, in turn, increases the level of Lamp1 at the plasma membrane, where it can be cleaved by IgA protease. Here, we show that porin also induces a Ca2+ flux in epithelial cells. This transient is similar in nature to that observed in phagocytes exposed to porin. In contrast to the pilus-induced Ca2+ transient, the porin-induced event does not trigger lysosome exocytosis. Instead, it stimulates exocytosis of early and late endosomes and increases Lamp1 on the cell surface. These results indicate that Neisseria pili and porin perturb Lamp1 trafficking in epithelial cells by triggering separate and distinct Ca2+-dependent exocytic events, bringing Lamp1 to the cell surface, where it can be cleaved by IgA protease.
机译：致病性奈瑟菌 spp分泌的免疫球蛋白A（IgA）蛋白酶。裂解Lamp1，从而改变细胞中的溶酶体并促进细菌细胞内存活。我们试图确定IgA蛋白酶如何获得进入细胞Lamp1的途径，以便更好地了解这种裂解事件在细菌感染中的作用。在以前的报告中，我们证明了菌毛诱导的Ca 2 + 瞬变触发人上皮细胞中的溶酶体胞吐作用。反过来，这会增加Lamp1在质膜的水平，在该处可以被IgA蛋白酶切割。在这里，我们表明孔蛋白还诱导上皮细胞中的Ca 2 + 通量。该瞬变本质上类似于暴露于孔蛋白的吞噬细胞中观察到的瞬变。与菌毛诱导的Ca 2 + 瞬变相反，孔蛋白诱导的事件不会触发溶酶体胞吐作用。相反，它刺激早期和晚期内体的胞吐作用，并增加细胞表面上的Lamp1。这些结果表明奈瑟菌菌毛和孔蛋白干扰Lamp1在上皮细胞中的运输，其方式是触发独立且独特的Ca 2 + 依赖的胞外事件，从而使Lamp1进入细胞表面，在那里可以被IgA蛋白酶切割。

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