Brawner D L, Mori M
Program in Infectious Diseases and Clinical Statistics, Fred Hutchinson Cancer Research Center, Seattle, Washington.
J Infect Dis. 1992 Sep;166(3):587-97. doi: 10.1093/infdis/166.3.587.
Host factors that influence binding of Candida albicans to murine spleen, lymph node, and kidney were studied. Organs were harvested from BALB/cByJ and AKR/J mice immunocompromised by irradiation, cyclophosphamide, and cortisone acetate alone or in combination. Tissues from treated mice and untreated littermates were compared for their ability to bind C. albicans in ex vivo assays. Immunosuppressive regimens decreased yeast binding to splenic marginal zones, but when mice recovered for 5 days after treatment, adherence to spleen was similar to adherence in untreated littermates. Adherence to lymph node and kidney in treated mice was not different from binding to these tissues in untreated mice. Total serum immunoglobulin titers correlated with binding of yeast cells to mouse spleen. Blocking studies ruled out a mannosyl-fucosyl receptor-mediated binding. These results suggest that ex vivo adherence of C. albicans represents a host immune defense mechanism by which the immunocompetent host binds blood-borne yeast cells to host immune cells in reticuloendothelial organs to prevent dissemination to other organs.
研究了影响白色念珠菌与小鼠脾脏、淋巴结和肾脏结合的宿主因素。从经单独或联合照射、环磷酰胺和醋酸可的松免疫受损的BALB/cByJ和AKR/J小鼠中获取器官。在体外试验中,比较了处理过的小鼠和未处理的同窝小鼠组织结合白色念珠菌的能力。免疫抑制方案降低了酵母与脾脏边缘区的结合,但当小鼠在治疗后恢复5天时,其对脾脏的黏附与未处理的同窝小鼠相似。处理过的小鼠对淋巴结和肾脏的黏附与未处理小鼠对这些组织的结合没有差异。血清总免疫球蛋白滴度与酵母细胞与小鼠脾脏的结合相关。阻断研究排除了甘露糖基-岩藻糖基受体介导的结合。这些结果表明,白色念珠菌的体外黏附代表了一种宿主免疫防御机制,通过该机制,具有免疫活性的宿主将血源酵母细胞与网状内皮器官中的宿主免疫细胞结合,以防止扩散到其他器官。