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首页> 外文期刊>Infection and immunity >Binding and Internalization of Glucuronoxylomannan, the Major Capsular Polysaccharide of Cryptococcus neoformans, by Murine Peritoneal Macrophages
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Binding and Internalization of Glucuronoxylomannan, the Major Capsular Polysaccharide of Cryptococcus neoformans, by Murine Peritoneal Macrophages

机译：葡糖醛酸氧甘露聚糖，新隐球菌的主要荚膜多糖，通过小鼠腹膜巨噬细胞的结合和内在化。

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Glucuronoxylomannan (GXM), the major component of the capsular polysaccharide of Cryptococcus neoformans, is essential to virulence of the yeast. Previous studies found that the interaction between GXM and phagocytic cells has biological consequences that may contribute to the pathogenesis of cryptococcosis. We found that GXM binds to and is taken up by murine peritoneal macrophages. Uptake is dose and time dependent. Examination of the sites of GXM accumulation by immunofluorescence microscopy showed that the pattern was discontinuous and punctate both on the surfaces of macrophages and at intracellular depots. Although resident macrophages showed appreciable accumulation of GXM, uptake was greatest with thioglycolate-elicited macrophages. A modest stimulation of GXM binding followed treatment of resident macrophages with phorbol 12-myristate 13-acetate, but treatment with lipopolysaccharide or gamma interferon alone or in combination had no effect. Accumulation of GXM was critically dependent on cytoskeleton function; a near complete blockade of accumulation followed treatment with inhibitors of actin. GXM accumulation by elicited macrophages was blocked by treatment with inhibitors of tyrosine kinase, protein kinase C, and phospholipase C, but not by inhibitors of phosphatidylinositol 3-kinase, suggesting a critical role for one or more signaling pathways in the macrophage response to GXM. Taken together, the results demonstrate that it is possible to experimentally enhance or suppress binding of GXM to macrophages, raising the possibility for regulation of the interaction between this essential virulence factor and binding sites on cells that are central to host resistance.
机译：新型隐球菌荚膜多糖的主要成分葡糖醛酸氧甘露聚糖（GXM）对酵母的毒性至关重要。先前的研究发现，GXM和吞噬细胞之间的相互作用具有生物学后果，可能会导致隐球菌病的发病。我们发现GXM与鼠腹膜巨噬细胞结合并被其吸收。摄取是剂量和时间依赖性。通过免疫荧光显微镜检查GXM积累的位点表明，该模式在巨噬细胞表面和细胞内贮库处都是不连续的且呈点状。尽管常驻巨噬细胞显示出明显的GXM积累，但是巯基乙酸盐诱导的巨噬细胞的摄取最大。用佛波醇12-肉豆蔻酸酯13-乙酸酯处理常驻巨噬细胞后，适度刺激GXM结合，但单独或联合使用脂多糖或γ干扰素治疗无效。 GXM的积累严重依赖于细胞骨架功能。用肌动蛋白抑制剂治疗后几乎完全阻止了蓄积。酪氨酸激酶，蛋白激酶C和磷脂酶C的抑制剂可阻止引起巨噬细胞的GXM积累，但磷脂酰肌醇3激酶的抑制剂则无法阻止GXM的积累，这表明一种或多种信号通路在巨噬细胞对GXM的应答中起着至关重要的作用。两者合计，结果表明，有可能通过实验增强或抑制GXM与巨噬细胞的结合，从而提高了调节这种必需毒力因子与宿主抗性中心细胞结合位点之间相互作用的可能性。

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