Regulatory effect of caspase-11 on interleukin-1β in the fungal keratitis.
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.
Department of Ophthalmology, Kaifeng Central Hospital, Kaifeng, Henan Province, China.
Keke
K
Zhu
Department of Ophthalmology, Kaifeng Central Hospital, Kaifeng, Henan Province, China.
Hongmei
H
Mu
Department of Ophthalmology, Kaifeng Central Hospital, Kaifeng, Henan Province, China.
Baimu
B
Pi
D033942:Adaptor Proteins, Vesicular Transport / Q000172:deficiency / Q000235:genetics; D000818:Animals; D001228:Aspergillosis / Q000201:enzymology* / Q000235:genetics / Q000276:immunology / Q000382:microbiology; D001232:Aspergillus fumigatus / Q000276:immunology / Q000472:pathogenicity*; D020170:Caspase 1 / Q000235:genetics / Q000378:metabolism*; D020169:Caspases / Q000378:metabolism*; D053471:Caspases, Initiator; D002478:Cells, Cultured; D003315:Cornea / Q000201:enzymology* / Q000276:immunology / Q000382:microbiology; D004195:Disease Models, Animal; D015821:Eye Infections, Fungal / Q000201:enzymology* / Q000235:genetics / Q000276:immunology / Q000382:microbiology; D005260:Female; D005838:Genotype; D054884:Host-Pathogen Interactions; D053583:Interleukin-1beta / Q000378:metabolism*; D007634:Keratitis / Q000201:enzymology* / Q000235:genetics / Q000276:immunology / Q000382:microbiology; D037181:Lectins, C-Type / Q000172:deficiency / Q000235:genetics; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009504:Neutrophils / Q000201:enzymology* / Q000276:immunology / Q000382:microbiology; D010641:Phenotype; D015398:Signal Transduction; D000072377:Syk Kinase / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000172:deficiency / Q000235:genetics; D000099181:Dectin-1
D033942:Adaptor Proteins, Vesicular Transport; D020170:Caspase 1; D020169:Caspases; D053471:Caspases, Initiator; D053583:Interleukin-1beta; D037181:Lectins, C-Type; D000072377:Syk Kinase; D051197:Toll-Like Receptor 4; D000099181:Dectin-1; C587672:IL1B protein, mouse; C476286:Ticam1 protein, mouse; C493487:Tlr4 protein, mouse; C000606897:Syk protein, mouse; C101136:Casp4 protein, mouse