ABSTRACT
Background Research determined that TLR4 is positively expressed on the macrophages in iris and ciliary in acute endotoxin-induced uveitis(EIU),indicating that TLR4 participated in the pathogenesis of the anterior uveitis.Objective The aim of this study is to observe the expressions of toll-like receptor-4(TLR4),Myeloid differentiation factor 88(MyD88),NF-κB p65 in iris tissue in the eyes with endotoxin-induced acute anterior uveitis.Methods Animal models of acute anterior uveitis were established by a hind footpad injection of 200μg Cholera vibrio LPS in 40 SPF Wistar rats with the age of 6-8 weeks.Other 10 age-matched rats were as normal controls.Ocular inflammation was examined under the slit lamp microscope at the 2-hour interval after the injection and intensity of inflammation was scored according to the standard of Lajavardi[4].Histopathology examination was performed for the evaluation of inflammatory reaction of iris and ciliary tissues by HE staining at 24 hours after LPS injection.Expressions of TLR4,MyD88 and NF-κB p65 in iris and ciliary body tissue were detected through immunohistochemistry.TLR4~+,MyD88~+ and NF-κB p65~+ cells were counted.Results The inflammatory reaction was gradually enhanced after injection of LPS and peaked at 24 hours and allivated 48 hours later.The infiltration of lots of inflammatory cells and fibrinous exudate were exhibited in the anterior chamber,posterior chamber,iris and ciliary tissue under the optical microscope at 24 hours after injection of LPS.No positive expressions of TLR4,MyD88 and NF-κB p65 in iris-ciliary body complex were found in normal control rats.The positive cells for TLR4,MyD88 and NF-κB p65 in iris-ciliary body complex were significantly different among 12 hours group,48 hours group and 72 hours groups(F=46.79,P＜0.05;F=54.37,P＜0.05;F=85.32,P＜0.05),and the positive cells for TLR4,MyD88 and NF-κB p65 peaked at 24 hours after injection of LPS.Conclusion The expression of TLR4 and its downstream signal transduction molecules MyD88,NF-κB p65 vary in uvea during EIU,indicating the potential role of LR4-MyD88 dependent pathway in the pathogenesis of acute anterior uveitis.