Studies on host defense mechanisms against mucocutaneous Candidia infection in mice

我们成功地建立了几种新的实验性口腔、咽、食管和阴道皮肤念珠菌病小鼠模型。建立这些念珠菌病模型的一个重要步骤包括给予氯丙嗪的镇静步骤，这有助于念珠菌的侵袭。白色念珠菌进入粘膜角质膜。口腔念珠菌病模型显示出类似人类自然感染的鹅口疮型发病机制，可用于真菌学和真菌学评价抗真菌治疗。通过使用该口腔念珠菌病模型，证明了牛乳铁蛋白、乳铁素、人唾液和几种草药制剂如茶树油通过口服给药的保护活性。特别是，重要的发现是乳铁蛋白对口腔念珠菌病的保护作用的机制与病变淋巴组织的T细胞活性的增强有关。我们还报道了从健康人制备的唾液，其中含有抑制念珠菌细胞附着于基质的蛋白质因子，对这种小鼠口腔念珠菌病也显示出保护作用。在阴道念珠菌病模型中，阴道分泌液中的保护性因子如髓过氧化物酶和乳铁蛋白可能起保护作用。

We successfully established several new experimental mucocutaneous candidiasis models in murine system, such as oral, pharyngeal, esophageal and vaginal candidiasis. An important procedure for establishment of these candidiasis models included a sedative step by administration of chlorpromazine which helped the invasion of C. albicans into mucocutenous membranes. Oral candidiasis model showed thrush-type pathogenesis that mimics the natural infection in humans and is useful for both symptomatological and mycological evaluation of antifungal treatments. By using this oral candidiasis model, the protective activities of bovine lactoferrin, lactoferricin, human saliva and several herbal preparations such as tea tree oil by oral administration were evidenced. Especially, important finding was that a mechanism of the protective actions of lactoferrin against oral candidiasis was associated with the augmentation of the T-cell activities of lesional lymphoid tissues. We also reported that saliva prepared from healthy persons, which contained proteinous factors inhibiting attachment of Candida cells to substratum, shows also protective action for this murine oral candidiasis. In the vaginal candidiasis model, protective factors, such as myeloperoxidase and lactoferrin in secretory fluids of vaginal cavity, were suggested to play a protective role.