真菌性角膜炎的分子机制研究进展

Molecular mechanism of fungal keratitis

真菌性角膜炎是严重危害视力的感染性角膜病。真菌黏附于角膜后，产生毒素及酶等物质损害角膜组织，而角膜对真菌的入侵产生免疫应答及炎症反应。基质金属蛋白酶在真菌性角膜炎中起着重要的作用。Toll样受体等模式识别受体对真菌的识别介导宿主角膜产生天然免疫和适应性免疫应答。在此过程中，众多的细胞、细胞因子及趋化因子参与了真菌的清除及角膜的损伤和修复。理清细胞之间的相互作用及信号转导，找到炎症反应及免疫反应的关键调控分子，是真菌性角膜炎防治的前提。本文就真菌的黏附及毒素对受侵角膜的影响、角膜对真菌入侵的免疫应答及炎症应答等分子机制的研究进展进行综述。

Fungal keratitis, a common cause of corneal infectious diseases, is an important contributor to vision loss. Toxins and exoenzymes released from infiltrating fungi led to damage of the cornea. Matrix metalloproteinases played an important role in fungal keratitis. Recognition of fungi by pattern-recognition receptors such as Toll-like receptors mediated the host to produce initiate and adaptive immune responses. Immunoprotection and inflammatory reaction which include numerous cells, cytokines and chemokines were involved in the responses of cornea versus invading fungi. The cells and cytokines could protect cornea from fungi invasion but also cause some damage. The final outcome was depended upon the balance between impaired factors and repaired factors. A better understanding of molecular mechanism of the immunity and inflammation will provide new ideas for the treatment of fungal keratitis. The molecular mechanism of fungal keratitis was reviewed in this article.