Morphological transition in the human fungal pathogen Histoplasma capsulatum.
Morphological transition in the human fungal pathogen Histoplasma capsulatum.
复制标题
人类真菌病原体荚膜组织胞浆菌的形态转变。
DOI：
10.1016/0966-842x(94)90596-7
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发表时间：
1994
影响因子：
15.9
通讯作者：
Kobayashi,GS
中科院分区：
文献类型：
--
作者：
Maresca,B;Carratù,L;Kobayashi,GS
二形性真菌衣状组织胞浆菌是组织胞浆菌病的病原体，组织胞浆菌病是一种在世界范围内分布的呼吸道感染2。作为土壤中的腐生菌，它是菌丝体 (M)，但在易感宿主中作为寄生虫，它会变成芽殖酵母 (Y)。通过将温度从菌丝体时的 25℃ 转变为芽殖酵母时的 37℃，可以在体外可逆地复制这些形态阶段。菌丝到酵母（M+Y）的转化过程特别令人感兴趣，因为它是由温度升高触发的，并导致转化为有毒形式3。细胞介导的免疫对该疾病的病理生理学的重要性已被多项研究证明，这些研究表明，免疫特异性由淋巴细胞决定，杀微生物效应功能由宿主巨噬细胞决定。荚膜梭菌的培养物已从其流行的地理区域中回收，特别是从被蝙蝠和鸟类粪便污染的土壤中回收。活的菌丝体碎片和分生孢子通过空气传播并通过吸入进入肺道，然后真菌迅速传播到其他器官。在受感染的宿主中，H. capsdatum 遇到各种环境胁迫，它通过调节特定基因的表达来适应。作为一种病原体，它在网状内皮系统的吞噬细胞内存活，如果不及时治疗，它会导致易感宿主致命的感染。感染吞噬细胞的细胞内病原体（例如 H. capsdatum）会造成重要的健康问题，因为它们绕过宿主的主要防御机制：被专业吞噬细胞杀死和降解。
The dimorphic fungus Histoplasma capsdatum is the etiological agent of histoplasmosis, a respiratory infection that is worldwide in distribution2. As a saprophyte in soil it is mycelial (M), but it becomes a budding yeast (Y) as a parasite in susceptible hosts. These morphological phases can be reproduced reversibly in vitro by shifting the temperature from 25 C at which it is mycelial, to 37 C when it becomes a budding yeast. The process of mycelial-to-yeast(M+ Y) conversion is of particular interest since it is triggered by an increase in temperature and it leads to conversion to a virulent form3. The importance of cell-mediated immunity to the pathophysiology of this disease has been documented by several studies, which have shown that immune specificity is determined by lymphocytes4 and microbicidal effector function by host macrophages’.Cultures of H. capsulatum have been recovered from geographical areas in which it is endemic, particularly from soil contaminated by bat and bird droppings2. Viable mycelial fragments and conidia become airborne and enter the pulmonary tract by inhalation, after which the fungus rapidly disseminates to other organs. In the infected host, H. capsdatum encounters various environmental stresses to which it adapts by regulating the expression of specific genes. As a pathogen, it survives within phagocytic cells of the reticuloendothelial system and, if untreated, it causes fatal infections in susceptible hosts. Intracellular pathogens that infect phagocytic cells, such as H. capsdatum, pose important health problems because they circumvent a primary defence mechanism of the host: killing and degradation by professional phagocytic cell& ‘.