Sakai Kanae, Hiemori Keiko, Tateno Hiroaki, Hirabayashi Jun, Gonoi Tohru
Medical Mycology Research Center, Chiba University, Japan.
Department of Life Science and Biotechnology, Biotechnology Research Institute for Drug Discovery, AIST, Japan.
Med Mycol. 2019 Jan 1;57(1):71-83. doi: 10.1093/mmy/myx163.
Aspergillus fumigatus is the major causative fungus of aspergillosis, and many studies have explored the relationship between A. fumigatus and pathogenicity. In the current study, we focused on a fucose-specific lectin, FleA, as a novel molecule which related to the pathogenicity of A. fumigatus. The disruption of the fleA gene did not lead to clear morphological changes compared to parental strain under several stress conditions in culture, but germination become earlier. In comparison with parental strain, the pathogenicity of disruptant was enhanced in a mouse infection model. The pattern of conidial phagocytosis and adhesion to cultured cells did not explain this enhanced pathogenicity. FleA was reported to contain six conserved fucose-binding sites; the analysis of constructed FleA point mutants revealed nonequivalent contribution of the fucose-binding sites to fucose binding. Based on the immune response induced in the cultured cells upon exposure to wild-type and mutant FleA, we propose a model of the FleA molecule in A. fumigatus infection.
烟曲霉是曲霉病的主要致病真菌，许多研究探讨了烟曲霉与致病性之间的关系。在本研究中，我们聚焦于一种岩藻糖特异性凝集素FleA，它是一种与烟曲霉致病性相关的新分子。与亲本菌株相比，在几种培养应激条件下，fleA基因的破坏并未导致明显的形态变化，但萌发提前。与亲本菌株相比，缺失突变体在小鼠感染模型中的致病性增强。分生孢子的吞噬模式和对培养细胞的粘附并不能解释这种增强的致病性。据报道，FleA含有六个保守的岩藻糖结合位点；对构建的FleA点突变体的分析表明，岩藻糖结合位点对岩藻糖结合有不同的贡献。基于野生型和突变型FleA暴露后培养细胞中诱导的免疫反应，我们提出了一个烟曲霉感染中FleA分子的模型。
