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首页> 外文期刊>Infection and immunity >Binding of Serum Mannan Binding Lectin to a Cell Integrity-Defective Cryptococcus neoformans ccr4Δ Mutant
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Binding of Serum Mannan Binding Lectin to a Cell Integrity-Defective Cryptococcus neoformans ccr4Δ Mutant

机译：血清甘露聚糖结合凝集素与细胞完整性缺陷型隐球菌ccr4Δ突变体的结合。

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摘要

Mannan binding lectin (MBL) is an innate immune mediator belonging to the collectin family known to bind to the surfaces of many viruses, bacteria, and fungi. However, pathogenic strains of the fungus Cryptococcus neoformans are resistant to MBL binding. To dissect the mechanism of cryptococcal resistance to MBL, we compared MBL binding to an encapsulated wild-type strain, an encapsulated ccr4Δ mutant defective in cell integrity, and an acapsular cap60Δ strain. No MBL binding was detected on wild-type C. neoformans. In contrast, the ccr4Δ mutant bound MBL to the cell wall, predominantly at the ends of enlarged buds, whereas the acapsular strain bound MBL only at the bud neck and bud scars. In addition, the ccr4Δ mutant was sensitive to the cell wall-active antifungal caspofungin and other cell wall stress inducers, and its virulence was reduced in a mouse model of cryptococcosis. Interestingly, treatment of wild-type cells with caspofungin also increased MBL binding to C. neoformans. These results suggest that both the presence of capsule and wild-type cell wall architecture preclude MBL binding to C. neoformans.
机译：甘露聚糖结合凝集素（MBL）是一种固有的免疫介质，属于collectin家族，已知与许多病毒，细菌和真菌的表面结合。然而，真菌新隐球菌的致病性菌株对MBL结合具有抗性。为了剖析隐球菌对MBL的抗性机制，我们比较了MBL与封装的野生型菌株，封装的细胞完整性缺陷的 ccr4 Δ突变体和封装的 cap60 的结合力。 Δ应变。在野生型 C上未检测到MBL结合。新甲虫。相反， ccr4 Δ突变体将MBL结合在细胞壁上，主要在扩大的芽的末端，而荚膜菌株仅在芽颈和芽疤处结合MBL。此外， ccr4 Δ突变体对细胞壁活性抗真菌卡泊芬净和其他细胞壁应激诱导剂敏感，并且在隐球菌病小鼠模型中其毒性降低。有趣的是，用卡泊芬净治疗野生型细胞也增加了MBL与 C的结合。新甲虫。这些结果表明，胶囊和野生型细胞壁结构的存在都排除了MBL与 C的结合。新甲虫。

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