De Bernardis F, Boccanera M, Adriani D, Spreghini E, Santoni G, Cassone A
Department of Bacteriology and Medical Mycology, Istituto Superiore di Sanità, Rome, Italy.
Infect Immun. 1997 Aug;65(8):3399-405. doi: 10.1128/iai.65.8.3399-3405.1997.
The role of antibodies (Abs) in the resistance to vaginal infection by Candida albicans was investigated by using a rat vaginitis model. Animals receiving antimannoprotein (anti-MP) and anti-aspartyl proteinase (Sap) Ab-containing vaginal fluids from rats clearing a primary C. albicans infection showed a highly significant level of protection against vaginitis compared to animals given Ab-free vaginal fluid from noninfected rats. Preabsorption of the Ab-containing fluids with either one or both proteins MP and Sap sequentially reduced or abolished, respectively, the level of protection. A degree of protection against vaginitis was also conferred by postinfectious administration of anti-Sap and anti-MP monoclonal antibodies (provided the latter were directed against mannan rather than protein epitopes of MP) and by intravaginal immunization with a highly purified, polysaccharide-free Sap preparation. Postinfectious administration of pepstatin A, a potent Sap inhibitor, greatly accelerated the clearance of C. albicans from rat vagina. No anti-MP or anti-Sap Abs were elicited during a C. albicans vaginal infection of congenitally athymic nude rats. Although they were as able as their euthymic counterparts to clear the primary infection, these animals did not show increased resistance to a rechallenge, demonstrating that induction of anticandidal protection in normal rats was a thymus-dependent Ab response. Overall, our data strengthen the concept that Abs against some defined Candida antigens are relevant in the mechanism of acquired anticandidal protection in vaginitis. The T-cell dependence of this protection may also provide a link between cell-mediated and humoral immunity in vaginal infection.
通过使用大鼠阴道炎模型，研究了抗体（Abs）在抵抗白色念珠菌阴道感染中的作用。与给予来自未感染大鼠的无抗体阴道液的动物相比，接受来自清除原发性白色念珠菌感染的大鼠的含抗甘露糖蛋白（抗MP）和抗天冬氨酸蛋白酶（Sap）抗体的阴道液的动物对阴道炎具有高度显著的保护水平。用MP和Sap这两种蛋白质中的一种或两种依次预吸收含抗体的液体，分别降低或消除了保护水平。感染后给予抗Sap和抗MP单克隆抗体（前提是后者针对甘露聚糖而非MP的蛋白质表位）以及用高度纯化的无多糖Sap制剂进行阴道内免疫，也赋予了一定程度的抗阴道炎保护作用。感染后给予强效Sap抑制剂胃蛋白酶抑制剂A，大大加速了白色念珠菌从大鼠阴道的清除。在先天性无胸腺裸鼠的白色念珠菌阴道感染期间未诱导出抗MP或抗Sap抗体。尽管它们与有胸腺的同类动物一样能够清除原发性感染，但这些动物对再次感染并未表现出增强的抵抗力，这表明正常大鼠中抗念珠菌保护的诱导是一种胸腺依赖性抗体反应。总体而言，我们的数据强化了这样一种观念，即针对某些特定念珠菌抗原的抗体与阴道炎中获得性抗念珠菌保护机制相关。这种保护的T细胞依赖性也可能在阴道感染中细胞介导免疫和体液免疫之间提供联系。
