Ollert M W, Wadsworth E, Calderone R A
Department of Microbiology, Georgetown University Medical Center, Washington, D.C. 20007.
Infect Immun. 1990 Apr;58(4):909-13. doi: 10.1128/iai.58.4.909-913.1990.
Pseudohyphae of Candida albicans bear surface receptors for iC3b and C3d. In order to determine a possible role for these receptors in the pathogenesis of candidiasis, a spontaneous C. albicans mutant, m-10, which exhibits reduced ability to adhere in vitro to fibrin platelet clots and epithelial cells or to cause endocarditis in a rabbit model, and its parent wild-type (wt) strain were compared for receptor expression in rosetting assays with sheep erythrocytes carrying iC3b (EAC1423bi) or C3d (EAC1423d). An equally high attachment to wt and m-10 was seen with EAC1423d, whereas rosetting with EAC1423bi was reduced by 53% in m-10 compared with wt. In inhibition studies, rosetting of wt with EAC1423bi was markedly inhibited by culture filtrate, hyphal-cell extract, and DEAE-fractionated material prepared from wt (54, 87, and 70% decreases in rosetting, respectively), thus suggesting the presence of the soluble, functionally active iC3b receptor of C. albicans in each of these preparations. Minimal inhibition of iC3b rosetting, however, was seen with the identical materials from m-10 (21, 5, and 12%, respectively). All of the preparations from the two strains were equally effective in their inhibitory activities against rosetting of C3d. A human serum specimen obtained from a patient with chronic mucocutaneous candidiasis blocked iC3b rosetting of the wt strain almost completely. When used in an immunoblot, this serum recognized proteins of 68 to 71, 55, and 50 kilodaltons (kDa) in hyphal-cell extracts of the wt. With the same preparation of the avirulent mutant, only weak reactions with the 68- to 71-kDa and 55-kDa proteins occurred, while the 50-kDa protein was not detectable. Taken together, these results indicate that the expression of the functionally active iC3b receptor on C. albicans may be involved in the virulence of the organism, possibly by mediating adherence to mammalian cells.
白色念珠菌的假菌丝带有iC3b和C3d的表面受体。为了确定这些受体在念珠菌病发病机制中的可能作用,将一株自发的白色念珠菌突变体m-10及其亲本野生型(wt)菌株进行比较,m-10在体外对纤维蛋白血小板凝块和上皮细胞的黏附能力以及在兔模型中引起心内膜炎的能力均有所降低。在与携带iC3b(EAC1423bi)或C3d(EAC1423d)的绵羊红细胞进行的玫瑰花结试验中比较了它们的受体表达。EAC1423d对wt和m-10的黏附程度相同,而与EAC1423bi形成的玫瑰花结在m-10中比wt减少了53%。在抑制研究中,wt与EAC1423bi形成的玫瑰花结受到培养滤液、菌丝细胞提取物以及从wt制备的DEAE分级材料的显著抑制(玫瑰花结分别减少54%、87%和70%),这表明在这些制剂中均存在白色念珠菌的可溶性、功能活性iC3b受体。然而,来自m-10的相同材料对iC3b玫瑰花结的抑制作用最小(分别为21%、5%和12%)。两种菌株的所有制剂对C3d玫瑰花结的抑制活性相同。从一名慢性黏膜皮肤念珠菌病患者获得的一份人血清标本几乎完全阻断了wt菌株的iC3b玫瑰花结形成。当用于免疫印迹时,该血清在wt的菌丝细胞提取物中识别出68至71 kDa、55 kDa和50 kDa的蛋白质。对于无毒力突变体的相同制剂,仅与68至71 kDa和55 kDa的蛋白质发生微弱反应,而未检测到50 kDa的蛋白质。综上所述,这些结果表明白色念珠菌上功能活性iC3b受体的表达可能参与了该生物体的毒力,可能是通过介导对哺乳动物细胞的黏附来实现的。