| Background:Pathogenesis of acute angle-closure glaucoma is not entirely clear, eye abnormalit-ies such as shallow central anterior chamber depth (ACD),narrow angle,a thicklen,short axial length and cornea radius, has been recognized mainly risk factors ofthe disease,but only some of the people with these anatomical features with acuteangle-closure glaucoma.Recent studies show that the body’s Immune regulatingfunction are closely related with the onset of glaucoma.Toll-like receptors play animportant role in the immune processes in the body,it not only has a critical role ininnate immunity after pathogen infection,but also triggers an immune response bybinding endogenous ligands in aseptic injury. Many tissues in eyes including humancornea,conjunctiva,iris,ciliary body,uvea,retina,and so on can express Toll-likereceptors. So far,Toll-like receptors that found by humans are11kinds,however, inwhich the TLR4is found that the earliest and it is the most studied.Trauma andinfection with the same mediators at the molecular level in the processes of causinginflammatory reactions.Post-traumatic stress or degradation of the cells result in therelease or secretion of certain substances,these substances combined with TLR4,viaMyD88-dependent pathway or MyD88-independent pathway,play a role in theimmune process in the body.The present study was set to measure the expression ofTLR4and MyD88in the iris of patients with the acute angle-closure glaucoma acuteexacerbation,and to explore the pathogenesis of acute angle-closure glaucoma atimmunological and molecular level.Objective：TO investigate the differences between expression of Toll-like receptor4(TLR4)and myeloid differentiation factor88(MyD88) in iris of patients with acute angle-closure glaucoma with acute attack and normal person.To study therelationship between the pathogenesis of acute angle-closure glaucoma and TLR4MyD88-dependent signaling pathways,which contribute to providing a theoreticalbasis to find a effective way to prevent and treat acute angle-closure glaucoma in theclinical.Methods：Control group:20control subjects that iris of organ donors with no eye diseases;the experimental group: Iris of60patients with acute angle-closure glaucoma withacute attack be cut off in compound trabeculectomy.Changes of iris tissuemorphology of the two study groups were measured by HE staining; The changes ofexpression of TLR4and MyD88and TLR4and MyD88cells distribution contained intwo iris tissue groups were measured using immunofluorescence; Western Blotdetects changes of TLR4and MyD88receptor protein expression in iris between twostudy groups.Results：HE staining showed that: the experimental group compared with the control group,the iris tissue fibers enlarged and blood vessels dilated significantly,besides,macrophages in the visible blood vessels and tissues are significantlyincreased; Immunofluorescence outcomes showed: Both of the experimental groupand the control group express TLR4and MyD88in iris,and TLR4and MyD88cellsmainly contained in the iris epithelium and stroma.TLR4is mainly expressed on thecell membrane, while MyD88mainly expressed in the cytoplasm; experimental groupiris tissue expression of TLR4and MyD88significantly higher than that of controlgroup by optical density analysis integrating the results statistically,so there wasstatistically significant difference; Western Blot show: the expression of TLR4andMyD88of the experimental group significantly higher than that of control groupthrough the gray analysis,the difference was statistically significant.Conclusion： Iris tissue of patients with acute angle-closure glaucoma with acute attack induceaseptic inflammation reaction; the expression levels of TLR4and MyD88significantly increased in iris of patients with acute angle-closure glaucoma with acuteattack,there may be certern relations between acute angle-closure glaucoma with acuteattack and the immunomodulation of TLR4and MyD88which may followTLR4-MyD88-dependent signaling pathways. |
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