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Evidence for macrophage-mediated protection against lethal Candida albicans infection.巨噬细胞介导的针对致死性白色念珠菌感染的保护作用的证据。
Infect Immun. 1986 Feb;51(2):668-74. doi: 10.1128/iai.51.2.668-674.1986.
2
Immunomodulation by Candida albicans: crucial role of organ colonization and chronic infection with an attenuated agerminative strain of C. albicans for establishment of anti-infectious protection.白色念珠菌的免疫调节作用:器官定植及白色念珠菌减毒无芽管菌株慢性感染在建立抗感染保护中的关键作用。
J Gen Microbiol. 1988 Sep;134(9):2583-92. doi: 10.1099/00221287-134-9-2583.
3
Role of L3T4+ lymphocytes in protective immunity to systemic Candida albicans infection in mice.L3T4⁺淋巴细胞在小鼠全身性白色念珠菌感染保护性免疫中的作用。
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Immunomodulation by a low-virulence, agerminative variant of Candida albicans. Further evidence for macrophage activation as one of the effector mechanisms of nonspecific anti-infectious protection.白色念珠菌低毒力、无芽变体的免疫调节作用。巨噬细胞激活作为非特异性抗感染保护效应机制之一的进一步证据。
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Immune Protection against Lethal Fungal-Bacterial Intra-Abdominal Infections.免疫保护对抗致命真菌-细菌腹腔内感染。
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ACQUIRED IMMUNITY TO CANDIDIASIS IN MICE.小鼠对白念珠菌的获得性免疫
J Bacteriol. 1963 Sep;86(3):401-6. doi: 10.1128/jb.86.3.401-406.1963.
2
Pathogenicity of Candida.念珠菌的致病性。
J Bacteriol. 1961 Apr;81(4):550-6. doi: 10.1128/jb.81.4.550-556.1961.
3
Cellular mechanisms underlying the adjuvant activity of Candida albicans in a mouse lymphoma model.白色念珠菌在小鼠淋巴瘤模型中的佐剂活性的细胞机制。
Int J Cancer. 1982 Apr 15;29(4):483-8. doi: 10.1002/ijc.2910290420.
4
Experimental vaccination with Candida albicans ribosomes in cyclophosphamide-treated animals.在环磷酰胺处理的动物中用白色念珠菌核糖体进行实验性疫苗接种。
Sabouraudia. 1981 Dec;19(4):267-73.
5
Absence of correlation between delayed-type hypersensitivity and protection in experimental systemic candidiasis in immunized mice.免疫小鼠实验性系统性念珠菌病中迟发型超敏反应与保护作用之间无相关性。
Infect Immun. 1981 Jan;31(1):95-101. doi: 10.1128/iai.31.1.95-101.1981.
6
Effects of cyclophosphamide on murine candidiasis.环磷酰胺对小鼠念珠菌病的影响。
Infect Immun. 1980 Feb;27(2):376-86. doi: 10.1128/iai.27.2.376-386.1980.
7
Experimental murine candidiasis: cell-mediated immunity after cutaneous challenge.实验性小鼠念珠菌病:皮肤激发后的细胞介导免疫
Infect Immun. 1980 Jan;27(1):140-9. doi: 10.1128/iai.27.1.140-149.1980.
8
A glycolipid on the surface of mouse natural killer cells.小鼠自然杀伤细胞表面的一种糖脂。
Eur J Immunol. 1980 Mar;10(3):175-80. doi: 10.1002/eji.1830100304.
9
A radiolabel release microassay for phagocytic killing of Candida albicans.
J Immunol Methods. 1982 Aug 13;52(3):369-77. doi: 10.1016/0022-1759(82)90008-4.
10
Induction of germ tube formation by N-acetyl-D-glucosamine in Candida albicans: uptake of inducer and germinative response.N-乙酰-D-葡萄糖胺诱导白色念珠菌形成芽管:诱导剂的摄取和发芽反应。
J Bacteriol. 1982 Nov;152(2):555-62. doi: 10.1128/jb.152.2.555-562.1982.

巨噬细胞介导的针对致死性白色念珠菌感染的保护作用的证据。

Evidence for macrophage-mediated protection against lethal Candida albicans infection.

作者信息

Bistoni F, Vecchiarelli A, Cenci E, Puccetti P, Marconi P, Cassone A

出版信息

Infect Immun. 1986 Feb;51(2):668-74. doi: 10.1128/iai.51.2.668-674.1986.

DOI:10.1128/iai.51.2.668-674.1986
PMID:3943907
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC262402/
Abstract

Systemic infection of mice with a Candida albicans strain (PCA-2) incapable of yeast-mycelial conversion conferred protection against a subsequent intravenous challenge with the pathogenic strain of the parent organism, strain CA-6. Protection was nonspecific since it was also detected upon challenge of mice with Staphylococcus aureus. Moreover, the PCA-2 organisms had to be viable, their effects being most evident when they were given intravenously at a dose of 10(6) cells 7 to 14 days prior to microbial challenge. Thus, all mice pretreated with PCA-2 and challenged 14 days later with viable CA-6 cells lived through a 60-day observation period, whereas all control mice not treated with PCA-2 died within 3 days. In an attempt to correlate the immunostimulatory effects observed in vivo with possible modifications in in vitro functions, it was found that administration of PCA-2 was accompanied by an increase in the number of peripheral blood polymorphonuclear cells and by the activation in the spleen of cells with highly candidacidal activity in vitro. Moreover, the adoptive transfer of plastic-adherent cells from PCA-2-infected mice into histocompatible recipients conferred considerable protection against subsequent CA-6 challenge.

摘要

用一种无法进行酵母-菌丝体转变的白色念珠菌菌株(PCA-2)对小鼠进行全身感染,可使其免受亲本菌株CA-6致病菌株随后的静脉内攻击。这种保护是非特异性的,因为在用金黄色葡萄球菌攻击小鼠时也能检测到。此外,PCA-2微生物必须是活的,当它们在微生物攻击前7至14天以10(6)个细胞的剂量静脉注射时,其效果最为明显。因此,所有用PCA-2预处理并在14天后用活的CA-6细胞攻击的小鼠都度过了60天的观察期,而所有未用PCA-2处理的对照小鼠在3天内死亡。为了将体内观察到的免疫刺激作用与体外功能的可能改变联系起来,发现给予PCA-2会伴随着外周血多形核细胞数量的增加以及体外具有高度杀念珠菌活性的脾脏细胞的激活。此外,将来自PCA-2感染小鼠的塑料贴壁细胞过继转移到组织相容性受体中,可对随后的CA-6攻击提供相当大的保护。