Bonnin Alain
Laboratoire de parasitologie-mycologie, Plateau Technique de Biologie, CHU, 2, rue Angélique Ducoudray, BP 37013, 21070 Dijon cedex.
Bull Acad Natl Med. 2012 Jan;196(1):139-49.
Invasive fungal infections (IFI) have become a major public health problem in industrialized countries, notably due to the increasing number of immunocompromized individuals. Endogenous candidiasis, arising from the patient's commensal flora, accounts for the majority of IFI. C albicans, generally originating from the colonized gastrointestinal tract, is the causative agent in about 50% of cases. Molecular and cellular investigations are helping to decipher the mechanisms underlying the commensal-pathogen transition. We have found that neutropenic patients are generally colonized by a single genotype, and that all C. albicans genotypes can cause invasive infection. By using epithelial cell-based models, we have shown that alpha 1, 2 and beta 1, 2 mannosides present in the outermost layer of the fungal cell wall mediate adherence to enterocytes. In addition, C. albicans uses different strategies for epithelial cell invasion, depending on the precise cell type with which it interacts.
侵袭性真菌感染（IFI）在工业化国家已成为一个主要的公共卫生问题，尤其是由于免疫功能低下个体数量的增加。内源性念珠菌病源于患者的共生菌群，占IFI的大多数。白色念珠菌通常起源于定植的胃肠道，约50%的病例由其引起。分子和细胞研究有助于解读共生菌向病原体转变的潜在机制。我们发现，中性粒细胞减少的患者通常被单一基因型定植，且所有白色念珠菌基因型都可引起侵袭性感染。通过使用基于上皮细胞的模型，我们表明真菌细胞壁最外层存在的α1,2和β1,2甘露糖苷介导了与肠上皮细胞的黏附。此外，白色念珠菌根据与其相互作用的具体细胞类型，采用不同策略侵袭上皮细胞。
