Expression Of MIP-2,MMP-2 And TIMP-2 In Rabbit Model Of Acanthamoeba Keratitis

【Abstract】:Purpose:To establish an effective animal model of acanthamoeba keratitis in rabbit, detect the expression of macrophage inflammatory protein 2(MIP-2),matrix metalloproteinase 2(MMP-2) and its tissue inhibitor 2(TIMP-2) in acanthamoeba keratitis, investigate the function of MIP-2,MMP-2 and TIMP-2 in the pathogenesy of acanthamoeba keratitis.Methods: Acanthamoeba keratitis was produced in 30 eyes from 30 New Zealand white rabbits by"epikeratophakia with the aid of corneal epthelium erasion".The expression and distribution of MIP-2,MMP-2 and TIMP-2 in corneal were tested with immunohistochemical dying. The results were analyzed by using coputer analysis system.Results: The expression of MIP-2 was mainly located in corneal epithelium and stroma in the experimental groups, and no expression of that was detected in control group. The level of MIP-2 increased with time-lapse.The level of MIP-2 reached its peak 5 days after infection, then its level began to decrease. The expession of MMP-2,TIMP-2 were mainly lacated in corneal stroma in both control group and experimental groups. The level of MMP-2,TIMP-2 reached their peaks 9 days after infection. The level of MMP-2 was higher than that of TIMP-2 in experimental groups.Conclusion: High expression of MIP-2 at the early stage of acanthamoeba keratitis was positively correlated with the extent of acanthamoeba infection.This result indicated that, as a chemotactic factor ,MIP-2 played an important role in the process of acanthamoeba keratitis. MMP-2 , TIMP-2 were involved in the corneal rehabilitation.The expression imbalance between MMP-2 and TIMP-2 may paly a critical role in the pathogenesis of corneal ulceration and nevascularization.