Millions of hibernating bats across North America have died from white-nose syndrome (WNS), an emerging disease caused by a psychrophilic (cold-loving) fungus, Pseudogymnoascus destructans , that invades their skin. Mechanisms of P. destructans invasion of bat epidermis remain obscure. Guided by our in vivo observations, we modeled hibernation with a newly generated little brown bat ( Myotis lucifugus ) keratinocyte cell line. We uncovered the stealth intracellular lifestyle of P. destructans , which inhibits apoptosis of keratinocytes and spreads through the cells by two epidermal growth factor receptor (EGFR)–dependent mechanisms: active penetration during torpor and induced endocytosis during arousal. Melanin of endocytosed P. destructans blocks endolysosomal maturation, facilitating P. destructans survival and germination after return to torpor. Blockade of EGFR aborts P. destructans entry into keratinocytes.

中文翻译：

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冬眠蝙蝠休眠和觉醒期间破坏拟裸囊菌的致病策略


北美数以百万计的冬眠蝙蝠死于白鼻综合症（WNS），这是一种由嗜冷（喜冷）真菌引起的新疾病，破坏拟裸子囊菌，侵入他们的皮肤。机制破坏假单胞菌蝙蝠表皮的入侵仍不清楚。在我们的体内观察的指导下，我们用新生成的小棕色蝙蝠模拟了冬眠（鼠耳蝠）角质形成细胞系。我们发现了隐秘的细胞内生活方式破坏假单胞菌，它抑制角质形成细胞的凋亡，并通过两种表皮生长因子受体（EGFR）依赖性机制在细胞中扩散：休眠期间的主动渗透和唤醒期间诱导的内吞作用。内吞黑色素破坏假单胞菌阻断内溶酶体成熟，促进破坏假单胞菌恢复休眠后的存活和发芽。 EGFR 的阻断中止破坏假单胞菌进入角质形成细胞。