Activation Of NLRP3 Inflammatory Bodies And Its Mechanism Of Action In The Innate Immunity Of Fungal Keratitis

Objective : To investigate the inflammatory effects of Nod-like receptor protein-3(NLRP3)inflammasome and the influence to IL-1?the downstream factor in the cultured tolerated human cornea epithelial cells(HCECs)stimulated with the Aspergillus fumigatus(A.fumigatus).Methods: The experiment is divided into two parts.(1)Real-time PCR and Wesstern blot were used to dectect the expression of NLRP3 inflammasome in the normal and infected HCECs which were challenged with A.fumigatus hypha..(2)HCECs were pre-treated with Glyburide for 2 hours before challenged with A.fumigatus hypha.Real-time PCR,Wesstern blot were used to exam the expression of NLRP3.Enzyme-linked immunosorbent assay(ELISA)were used to exam the expression of IL-1?.Results: NLRP3 inflammasome was expressed in HCECs.The NLRP3 inflammasome expression increased when stimulated with A.fumigatus hypha in time-dependent manner.The HCECs were pretreated with Glyburide,the expressions all decreased.Glyburide suppressed the production of the inflammasome.Conclusion: These data demonstrate that the HCECs can produce NLRP3 inflammasome,,and the production of the cytokines can be increased by stimulation of A.fumigatus hypha.NLRP3 plays an important role in the early phase of recognizing A.fumigatus hypha antigen and induces the expressions of cytokines.NLRP3 inflammasome promotes the innate immune response indirectly.