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念珠菌病的发病机制。细胞壁甘露聚糖分解代谢产物导致的免疫抑制。

Pathogenesis of candidiasis. Immunosuppression by cell wall mannan catabolites.

作者信息

Podzorski R P, Herron M J, Fast D J, Nelson R D

机构信息

Department of Microbiology, University of Minnesota, Minneapolis.

出版信息

Arch Surg. 1989 Nov;124(11):1290-4. doi: 10.1001/archsurg.1989.01410110044009.

DOI:10.1001/archsurg.1989.01410110044009
PMID:2684094
Abstract

Candida albicans cell wall mannan polysaccharide has an ability to negatively influence cell-mediated immune function. We have attempted to identify the mechanism of this phenomenon by testing the modulatory effects of isolated mannan and the chemical catabolites of mannan on cell-mediated immune function in vitro. We have determined that mannan isolated by complexation with cetyltrimethylammonium bromide (CTAB) is more antigenic than mannan isolated by precipitation with copper and that CTAB mannan does not inhibit lymphoproliferation stimulated by another antigen. We have also determined that oligosaccharides of three sizes, derived by chemical catabolism of CTAB mannan, are not antigenic, but instead are immunoinhibitory. Immunoinhibition does not involve interference with the mitogenic activity of interleukin 2. A similar occurrence of oligosaccharides may be produced by catabolism of mannan in vivo as evidenced by the presence of oligosaccharides of similar size in cell-free supernatant fluids derived from mononuclear leukocytes incubated with tritiated mannan. We propose that catabolites of fungal mannan may contribute significantly to suppression of cell-mediated immunity in candidiasis.

摘要

白色念珠菌细胞壁甘露聚糖多糖具有对细胞介导的免疫功能产生负面影响的能力。我们试图通过测试分离的甘露聚糖及其化学分解代谢产物对体外细胞介导的免疫功能的调节作用来确定这种现象的机制。我们已经确定,通过与十六烷基三甲基溴化铵(CTAB)络合分离得到的甘露聚糖比通过铜沉淀分离得到的甘露聚糖更具抗原性,并且CTAB甘露聚糖不会抑制由另一种抗原刺激的淋巴细胞增殖。我们还确定,由CTAB甘露聚糖化学分解产生的三种大小的寡糖没有抗原性,而是具有免疫抑制作用。免疫抑制不涉及对白介素2促有丝分裂活性的干扰。从与氚标记的甘露聚糖一起孵育的单核白细胞衍生的无细胞上清液中存在类似大小的寡糖证明,体内甘露聚糖的分解代谢可能产生类似的寡糖。我们提出,真菌甘露聚糖的分解代谢产物可能对念珠菌病中细胞介导免疫的抑制有显著贡献

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1
Pathogenesis of candidiasis. Immunosuppression by cell wall mannan catabolites.念珠菌病的发病机制。细胞壁甘露聚糖分解代谢产物导致的免疫抑制。
Arch Surg. 1989 Nov;124(11):1290-4. doi: 10.1001/archsurg.1989.01410110044009.
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Microbiol Immunol. 1996;40(2):125-31. doi: 10.1111/j.1348-0421.1996.tb03327.x.

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Candida albicans stimulates arachidonic acid liberation from alveolar macrophages through alpha-mannan and beta-glucan cell wall components.白色念珠菌通过α-甘露聚糖和β-葡聚糖细胞壁成分刺激肺泡巨噬细胞释放花生四烯酸。
Infect Immun. 1994 Aug;62(8):3138-45. doi: 10.1128/iai.62.8.3138-3145.1994.
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Clin Microbiol Rev. 1991 Jan;4(1):1-19. doi: 10.1128/CMR.4.1.1.
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