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首页> 外文期刊>Infection and immunity >Intravascular cryptococcal culture filtrate (CneF) and its major component, glucuronoxylomannan, are potent inhibitors of leukocyte accumulation.
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Intravascular cryptococcal culture filtrate (CneF) and its major component, glucuronoxylomannan, are potent inhibitors of leukocyte accumulation.

机译：血管内隐球菌培养物滤液（CneF）及其主要成分葡糖醛酸羟甘露聚糖是有效的白细胞蓄积抑制剂。

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Disseminated cryptococcosis is characterized by high titers of cryptococcal polysaccharides in serum and minimal cellular infiltrates in infected tissues of patients. The main objective of this study was to determine whether the circulating cryptococcal polysaccharides could contribute to the lack of cellular infiltration into infected tissues. To assess this possibility, a gelatin sponge implantation model was used. We found that intravenous (i.v.) injection of mice with cryptococcal culture filtrate antigen (CneF) inhibited migration of leukocytes (neutrophils, lymphocytes, and monocytes) into the intrasponge sites of acute inflammation induced by CneF, tumor necrosis factor alpha, or formylmethionyl leucyl phenylalanine. In addition, i.v. administration of CneF inhibited leukocyte migration into the intrasponge sites of a cell-mediated immune reaction irrespective of whether the delayed-type hypersensitivity response was to CneF or the mycobacterial antigen purified protein derivative. Glucuronoxylomannan, a major constituent of CneF and a major cryptococcal antigen detected in the sera of patients with disseminated cryptococcosis, when given i.v. to mice, inhibited leukocyte migration into the sponges. Our results suggest that the minimal cellular infiltrates observed in infected tissues of cryptococcosis patients may be due, in part, to the circulating cryptococcal polysaccharide functioning as we have demonstrated in the mouse model. Furthermore, the high titers of cryptococcal antigen in the sera of patients may diminish leukocyte migration in response to stimuli other than Cryptococcus neoformans, a point that may be relevant in AIDS patients with cryptococcosis.
机译：传播性隐球菌病的特征是血清中滴度高的隐球菌多糖和患者感染组织中的细胞浸润最少。这项研究的主要目的是确定循环中的隐球菌多糖是否可以导致缺乏向被感染组织的细胞浸润。为了评估这种可能性，使用了明胶海绵植入模型。我们发现静脉内（iv）注射隐球菌培养物滤液抗原（CneF）的小鼠抑制了白细胞（嗜中性粒细胞，淋巴细胞和单核细胞）迁移到由CneF，肿瘤坏死因子α或甲酰甲硫基亮氨酰苯丙氨酸诱导的急性炎症的海绵内部位。另外，i.v。不论延迟型超敏反应是对CneF还是对分枝杆菌抗原纯化的蛋白衍生物，施用CneF均可抑制白细胞迁移到细胞介导的免疫反应的海绵内部位。静脉内给予时，在散发性隐球菌病患者的血清中检测到了CneF的主要成分和主要的隐球菌抗原葡糖醛酸氧甘露聚糖。对小鼠而言，抑制了白细胞向海绵中的迁移。我们的结果表明，在隐球菌病患者的感染组织中观察到的最小细胞浸润可能部分归因于我们在小鼠模型中证明的循环隐球菌多糖功能。此外，患者血清中高滴度的隐球菌抗原可能会减少对新隐球菌以外的刺激的白细胞迁移，这一点可能与患有隐球菌的艾滋病患者有关。

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