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10
Phenotypic switching of Cryptococcus neoformans occurs in vivo and influences the outcome of infection.新型隐球菌的表型转换在体内发生,并影响感染结果。
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本文引用的文献

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Nonencapsulated Variant of Cryptococcus neoformans I. Virulence Studies and Characterization of Soluble Polysaccharide.新型隐球菌非包被变异株 I. 毒力研究及可溶性多糖的特性。
Infect Immun. 1971 Feb;3(2):287-94. doi: 10.1128/iai.3.2.287-294.1971.
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Tissue changes and tissue diagnosis in cryptococcosis; a study of 26 cases.隐球菌病的组织变化与组织诊断;26例研究
Am J Clin Pathol. 1955 Jan;25(1):14-24. doi: 10.1093/ajcp/25.1.14.
3
Virulence and growth rates of Cryptococcus neoformans in mice.新型隐球菌在小鼠体内的毒力和生长速率
Ann N Y Acad Sci. 1960 Aug 27;89:156-62. doi: 10.1111/j.1749-6632.1960.tb20138.x.
4
Macrophage nomenclature: where are we going?巨噬细胞命名法:我们将何去何从?
J Reticuloendothel Soc. 1980 Feb;27(2):223-45.
5
The capsule of cryptococcus neoformans passively inhibits phagocytosis of the yeast by macrophages.新型隐球菌的荚膜可被动抑制巨噬细胞对酵母的吞噬作用。
J Immunol. 1982 Oct;129(4):1675-80.
6
Roles of macrophage Fc and C3b receptors in phagocytosis of immunologically coated Cryptococcus neoformans.巨噬细胞Fc和C3b受体在免疫包被新型隐球菌吞噬作用中的作用。
Proc Natl Acad Sci U S A. 1981 Jun;78(6):3853-7. doi: 10.1073/pnas.78.6.3853.
7
Concomitant but not causal association between surface charge and inhibition of phagocytosis by cryptococcal polysaccharide.隐球菌多糖的表面电荷与吞噬作用抑制之间存在伴随但非因果的关联。
Infect Immun. 1980 Aug;29(2):295-300. doi: 10.1128/iai.29.2.295-300.1980.
8
Decreased virulence in stable, acapsular mutants of cryptococcus neoformans.新型隐球菌稳定无荚膜突变体的毒力降低。
Mycopathologia. 1982 Jul 23;79(1):23-9. doi: 10.1007/BF00636177.
9
Binding of cryptococcal polysaccharide to Cryptococcus neoformans.隐球菌多糖与新型隐球菌的结合。
Infect Immun. 1984 Mar;43(3):879-86. doi: 10.1128/iai.43.3.879-886.1984.
10
Sites of inhibition of mitochondrial electron transport in macrophage-injured neoplastic cells.巨噬细胞损伤的肿瘤细胞中线粒体电子传递的抑制位点。
J Cell Biol. 1982 Nov;95(2 Pt 1):527-35. doi: 10.1083/jcb.95.2.527.

新型隐球菌A血清型荚膜多糖抗吞噬活性的菌株变异

Strain variation in antiphagocytic activity of capsular polysaccharides from Cryptococcus neoformans serotype A.

作者信息

Small J M, Mitchell T G

机构信息

Department of Microbiology and Immunology, Duke University Medical Center, Durham, North Carolina 27710.

出版信息

Infect Immun. 1989 Dec;57(12):3751-6. doi: 10.1128/iai.57.12.3751-3756.1989.

DOI:10.1128/iai.57.12.3751-3756.1989
PMID:2680980
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC259900/
Abstract

Strains of Cryptococcus neoformans vary in resistance to phagocytosis in vitro. The binding of isolated capsular polysaccharide (CPS) to a capsule-free mutant of C. neoformans confers resistance to phagocytosis. The importance of capsule composition to differences among strains in susceptibility to phagocytosis was evaluated. CPSs from five strains of C. neoformans serotype A, designated 6, 15, 98, 110, and 145, which had previously been isolated and characterized as to molecular size, composition, and binding properties, were evaluated for relative antiphagocytic potencies. In the presence of 5% normal isologous serum, murine thioglycolate-elicited peritoneal macrophages phagocytized (i.e., attached to or engulfed) 80% of 51Cr-labeled cells of C. neoformans 602, a capsule-free mutant. Added CPS inhibited the uptake of these yeast cells. CPS from strain 110 was most potent, followed in decreasing order of inhibitory activity by CPSs from strains 6, 145, 98, and 15. The presence of 100 micrograms of strain 110 CPS per ml reduced uptake of cells of strain 602 from 80 to 50%. CPS had no effect on the uptake of 51Cr-labeled Saccharomyces cerevisiae. Cells of strain 602 that were preincubated with CPS and then washed were more resistant to phagocytosis than nonpretreated control cells, indicating the importance of bound, not free, CPS. Added CPS did not affect the uptake of wild-type, encapsulated cells of C. neoformans. Addition of endotoxin had no effect on phagocytosis. CPSs from strains of C. neoformans serotype A varied widely in their abilities to inhibit the uptake of capsule-free cells. The antiphagocytic activity of CPS did not correlate with the ability to bind to capsule-free mutant but was somewhat related to the capsule size of the strain from which the CPS was isolated.

摘要

新型隐球菌菌株在体外对吞噬作用的抗性存在差异。分离出的荚膜多糖(CPS)与新型隐球菌无荚膜突变体的结合赋予了对吞噬作用的抗性。评估了荚膜组成对不同菌株吞噬作用易感性差异的重要性。对先前已分离并在分子大小、组成和结合特性方面进行过表征的新型隐球菌血清型A的5个菌株(分别命名为6、15、98、110和145)的CPS进行了相对抗吞噬能力的评估。在5%正常同源血清存在的情况下,小鼠巯基乙酸诱导的腹腔巨噬细胞吞噬了(即附着于或吞噬了)80%的51Cr标记的新型隐球菌602无荚膜突变体细胞。添加的CPS抑制了这些酵母细胞的摄取。来自菌株110的CPS最有效,其次是来自菌株6、145、98和15的CPS,其抑制活性按降序排列。每毫升含有100微克菌株110 CPS可将菌株602细胞的摄取率从80%降低至50%。CPS对51Cr标记的酿酒酵母的摄取没有影响。预先用CPS孵育然后洗涤的菌株602细胞比未预处理的对照细胞对吞噬作用更具抗性,表明结合的而非游离的CPS的重要性。添加的CPS对新型隐球菌野生型有荚膜细胞的摄取没有影响。添加内毒素对吞噬作用没有影响。新型隐球菌血清型A菌株的CPS在抑制无荚膜细胞摄取的能力方面差异很大。CPS的抗吞噬活性与与无荚膜突变体结合的能力无关,但与分离CPS的菌株的荚膜大小有一定关系。