Carrow E W, Domer J E
Infect Immun. 1985 Jul;49(1):172-81. doi: 10.1128/iai.49.1.172-181.1985.
Immune regulation in candidiasis is inferred from studies of both human and animal infection, with a suppressive role suggested for cell wall polysaccharide. To study the immunosuppressive potential of Candida albicans in a murine model, whole blastoconidia or purified cell wall components of C. albicans were tested for their effects on the development of acquired immune responses by superimposing a pretreatment regimen upon an established immunization protocol. CBA/J or BALB/cByJ mice were pretreated twice intravenously with 100 micrograms of mannan (MAN), 100 or 200 micrograms of glycoprotein (GP), or 5 X 10(7) heat-killed C. albicans blastoconidia, followed 1 week later by an immunization protocol of two cutaneous inoculations of viable C. albicans blastoconidia given 2 weeks apart. Delayed hypersensitivity (DTH) to GP or to a membrane-derived antigen, B-HEX, was tested 7 days after the second inoculation, and lymphocyte stimulation was tested with mitogens and Candida antigens after 12 days. To assess protection, mice were challenged intravenously with viable C. albicans blastoconidia 14 days after the second cutaneous inoculation and sacrificed 28 days later for quantitative culture of kidneys and brains. Sera were obtained for enzyme-linked immunosorbent assays at selected intervals. Pretreatment with GP resulted in specific in vivo suppression of DTH to GP but not to B-HEX antigen and specific in vitro suppression of lymphocyte stimulation to GP but not to other Candida antigens or mitogens. MAN and heat-killed C. albicans blastoconidia had no such effects. GP pretreatment also diminished the protective effect of immunization against challenge, demonstrable in the brain, while not altering significantly the production of antibody in response to infection. Contrary to clinical evidence, MAN was not immunosuppressive in this model, and in fact, the immunosuppressive potential of GP, which is composed largely of MAN, was found to be dependent upon the presence of its heat-labile protein moiety.
念珠菌病中的免疫调节是通过对人类和动物感染的研究推断出来的，研究表明细胞壁多糖具有抑制作用。为了在小鼠模型中研究白色念珠菌的免疫抑制潜力，通过在既定的免疫方案上叠加预处理方案，测试了白色念珠菌的全芽生孢子或纯化的细胞壁成分对获得性免疫反应发展的影响。CBA/J或BALB/cByJ小鼠静脉内两次预处理100微克甘露聚糖（MAN）、100或200微克糖蛋白（GP）或5×10⁷个热灭活的白色念珠菌芽生孢子，1周后进行免疫方案，即两次皮肤接种活的白色念珠菌芽生孢子，间隔2周。在第二次接种后7天测试对GP或膜衍生抗原B-HEX的迟发型超敏反应（DTH），12天后用有丝分裂原和念珠菌抗原测试淋巴细胞刺激。为了评估保护作用，在第二次皮肤接种后14天，用活的白色念珠菌芽生孢子静脉内攻击小鼠，并在28天后处死，对肾脏和大脑进行定量培养。在选定的时间间隔采集血清进行酶联免疫吸附测定。用GP预处理导致体内对GP的DTH特异性抑制，但对B-HEX抗原无抑制，体外对GP的淋巴细胞刺激特异性抑制，但对其他念珠菌抗原或有丝分裂原无抑制。MAN和热灭活的白色念珠菌芽生孢子没有这种作用。GP预处理也降低了免疫对攻击的保护作用，在大脑中可得到证明，同时对感染后抗体的产生没有显著改变。与临床证据相反，MAN在该模型中没有免疫抑制作用，事实上，主要由MAN组成的GP的免疫抑制潜力被发现依赖于其热不稳定蛋白部分的存在。
