PATHOGENESIS OF CANDIDA INFECTIONS
PATHOGENESIS OF CANDIDA INFECTIONS
复制标题
DOI：
10.1016/s0190-9622(08)81257-1
复制
发表时间：
1994-09-01
影响因子：
13.8
通讯作者：
ODDS, FC
中科院分区：
文献类型：
--
作者：
ODDS, FC
皮肤和浅表粘膜部位的念珠菌感染是真菌毒力和宿主防御之间相互作用的结果。宿主表达表皮增殖和T淋巴细胞免疫应答以对抗真菌入侵，但炎症应答和非特异性抑制剂也可能发挥作用。白色念珠菌可以表达至少三种类型的表面粘附分子以定殖上皮表面，加上能够促进角化细胞的初始渗透的N-乙酰基蛋白酶。菌丝的形成有助于角化上皮细胞更深的渗透，C.白色念珠菌菌丝可以使用接触感应（触变性）作为引导机制。致病机制需要在该过程的每个新阶段毒力因子的差异表达：在C.因此，白色念珠菌可能是建立该物种相对高致病潜力的重要因素。
Candida infections of the skin and superficial mucosal sites are the result of an interplay be tween fungal virulence and host defenses. Epidermal proliferation and T-lymphocyte immune responses are expressed by the host to combat fungal invasion, but inflammatory responses and nonspecific inhibitors also probably play a role. Candida albicans can express at least three types of surface adhesion molecules to colonize epithelial surfaces, plus an aspartyl proteinase enzyme able to facilitate initial penetration of keratinized cells. Deeper penetration of keratinized epithelia is assisted by hypha formation, and C. albicans hyphae may use contact sensing (thigmotropism) as a guiding mechanism. Pathogenesis requires differential expression of virulence factors at each new stage of the process: a propensity for rapid alteration of the expressed phenotype in C. albicans may therefore be a significant factor in establishing the comparatively high pathogenic potential of this species.