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首页> 外文期刊>Infection and immunity >CNLAC1 Is Required for Extrapulmonary Dissemination of Cryptococcus neoformans but Not Pulmonary Persistence
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CNLAC1 Is Required for Extrapulmonary Dissemination of Cryptococcus neoformans but Not Pulmonary Persistence

机译：CNLAC1是新隐球菌肺外传播所必需的，而不是肺部持久性

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The pathogenic yeast Cryptococcus neoformans produces a laccase enzyme (CNLAC1), which catalyzes the synthesis of melanin in the presence of phenolic compounds. A number of genes have been implicated in the regulation of laccase and melanization, including IPC1, GPA1, MET3, and STE12. Albino mutants derived from random mutagenesis techniques may contain mutations in genes that regulate multiple virulence factors, including CNLAC1. The goal of our study is to investigate the role of CNLAC1 in virulence and evasion of pulmonary host defenses after infection via the respiratory tract. Using a set of congenic laccase-positive (2E-TUC-4) and laccase-deficient (2E-TU-4) strains, we found that both strains are avirulent at a lower dose (104 CFU/mouse) in mice. After the infectious dose was increased to 106 CFU/mouse, 70% mortality was observed in mice infected with 2E-TUC-4 compared to no mortality in mice infected with 2E-TU-4 at day 30 postinfection. This observation confirms the requirement for CNLAC1 in virulence. Interestingly, we observed no differences between the two strains in pulmonary growth or in elicitation of cellular immune responses in the lung. The only measurable defect of 2E-TU-4 was in dissemination to extrapulmonary sites. To examine the role of CNLAC1 in dissemination, mice were infected intravenously. By week 3 postinfection, equal numbers of strains 2E-TUC-4 and 2E-TU-4 were recovered from the brain and spleen. This observation indicates that CNLAC1 facilitates escape from the lung, but not growth in the lungs or brain, and suggests a novel role for CNLAC1 in virulence during an infection aquired via the respiratory tract.
机译：致病性酵母新型隐球菌产生漆酶（ CNLAC1 ），该酶在酚类化合物的存在下催化黑色素的合成。 IPC1 ， GPA1 ， MET3 和 STE12 涉及了许多漆酶和黑色素的调控基因。 em>。源自随机诱变技术的白化突变体可能包含调节多种毒力因子（包括 CNLAC1 ）的基因中的突变。我们的研究目的是研究 CNLAC1 在通过呼吸道感染后在毒力和逃避肺部宿主防御中的作用。使用一组同基因漆酶阳性（2E-TUC-4）和漆酶缺陷（2E-TU-4）菌株，我们发现这两种菌株在较低剂量（10 4 CFU）下均无毒。 /小鼠）。在将感染剂量增加至10 6 CFU /小鼠后，感染2E-TUC-4的小鼠观察到70％的死亡率，而第30天感染2E-TU-4的小鼠则没有死亡感染后。该观察结果证实了 CNLAC1 的毒性要求。有趣的是，我们在肺部生长或肺部细胞免疫应答的诱导中未观察到这两种菌株之间的差异。 2E-TU-4唯一可测量的缺陷是在肺外部位的传播。为了检查 CNLAC1 在传播中的作用，对小鼠进行静脉感染。感染后第3周，从大脑和脾脏中回收了相等数量的2E-TUC-4和2E-TU-4菌株。该观察结果表明， CNLAC1 有助于从肺中逃逸，但不能促进肺或脑中的生长，并且表明 CNLAC1 在通过呼吸道获得的感染过程中具有高毒力。道。

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