Zhu Keke, Mu Hongmei, Pi Baimu
Department of Ophthalmology, Kaifeng Central Hospital, Kaifeng, Henan Province, China.
Pak J Pharm Sci. 2016 Nov;29(6 Suppl):2327-2334.
Caused by fungus, fungal keratitis is a kind of infections corneal disease with high rate of blindness, which patients are mainly farmers in developing countries. Interleukin, as important proinflammatory cytokines, involve in immune defense process against fungal infection of cornea. The expression of interleukin in the pathogenesis of fungal keratitis, especially the main source of its cells, is not clear and the cell signaling pathways which regulate the synthesis and modification of interleukin is still unknown. Caspase-11 was obtained and cultured. And the ELISA and Western-blot methods were used to explore the regulatory effect of Caspse-11 on Interleukin-1β in the fungal keratitis. neutrophils were the main cell lineage of IL-1β to take part in the innate anti-fungi immunity in the cornea; IL-1β generation induced by fungal infection might not be through the pre-excitation in the classical signal pathway; TLR4/TRIF pathway was not involved in pro-IL-1β generation; while Dectin-1/syk pathway was involved in IL-1β generation in the fungal keratitis; Caspase-l participated in the modification of IL-1β to change from the precursor into the mature body; but NLRP3 inflammasome and ASC inflammasome were not involved in IL-1β generation; Caspase-11 was involved in IL-1β generation through regulating the modified process of Caspase-l to turning from precursor into mature body. TLR4/TRIF pathway and NLRP3 inflammasome and ASC inflammasome are not involved in the pro-IL-1β generation, while Caspase-l, Caspase-11 and Dectin-1/syk pathway are involved in the IL-1β generation.
真菌性角膜炎是由真菌引起的一种致盲率很高的感染性角膜疾病，患者主要是发展中国家的农民。白细胞介素作为重要的促炎细胞因子，参与角膜抗真菌感染的免疫防御过程。白细胞介素在真菌性角膜炎发病机制中的表达，尤其是其细胞的主要来源尚不清楚，调节白细胞介素合成和修饰的细胞信号通路仍不明确。获取并培养Caspase-11。采用酶联免疫吸附测定法（ELISA）和蛋白质免疫印迹法（Western-blot）探讨Caspase-11对真菌性角膜炎中白细胞介素-1β的调节作用。中性粒细胞是角膜中参与固有抗真菌免疫的白细胞介素-1β的主要细胞谱系；真菌感染诱导的白细胞介素-1β生成可能不是通过经典信号通路的预激活；Toll样受体4（TLR4）/TIR结构域衔接蛋白诱导干扰素β（TRIF）信号通路不参与白细胞介素-1β前体（pro-IL-1β）的生成；而C型凝集素受体1（Dectin-1）/脾酪氨酸激酶（syk）信号通路参与真菌性角膜炎中白细胞介素-1β的生成；半胱天冬酶-1（Caspase-1）参与白细胞介素-1β从前体转变为成熟体的修饰过程；但NOD样受体蛋白3（NLRP3）炎性小体和凋亡相关斑点样蛋白（ASC）炎性小体不参与白细胞介素-1β的生成；Caspase-11通过调节Caspase-1从前体转变为成熟体的修饰过程参与白细胞介素-1β的生成。TLR4/TRIF信号通路、NLRP3炎性小体和ASC炎性小体不参与pro-IL-1β的生成，而Caspase-1、Caspase-11和Dectin-1/syk信号通路参与白细胞介素-1β的生成。
