April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Research of Tlr4-myd88 Dependent Pathway in Endotoxin-Induced Uveitis
Author Affiliations & Notes
  • H. Lu
    Ophthalmology, Beijing Capital Medical University, Beijing, China
  • S. Li
    Ophthalmology, Beijing Capital Medical University, Beijing, China
  • F. X. Hu
    Ophthalmology, Beijing Capital Medical University, Beijing, China
  • W. Chen
    Ophthalmology, Beijing Capital Medical University, Beijing, China
  • Footnotes
    Commercial Relationships  H. Lu, None; S. Li, None; F.X. Hu, None; W. Chen, None.
  • Footnotes
    Support  National Nature Science Fund of China (30872361) and the National Key Technology R & D Program in the 11th Five Year Plan of China (2007BAI18B10)
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 1172. doi:
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      H. Lu, S. Li, F. X. Hu, W. Chen; Research of Tlr4-myd88 Dependent Pathway in Endotoxin-Induced Uveitis. Invest. Ophthalmol. Vis. Sci. 2010;51(13):1172.

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Abstract

Introduction: : The research of TLR4-MyD88 dependent pathway in Endotoxin-induced UvitisHong Lu, Shang Li, Xiaofeng Hu,Wei ChenDepartmnet of Ophthalmology, Beijing Chaoyang Hospital, Capital MedicalUniversity, No. 8 Baijiazhuang Road, Chaoyang District, Beijing, China, 100020;

Purpose: : To investigate the dynamics and distribution of Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), nuclear factor-kappa B p65 (NF-ΚB p65) and resident tissue macrophages in iris-ciliray tissue during endotoxin-induced uveitis (EIU) in Wistar rats.

Methods: : Wistar rats were randomly divided into 5 groups(0h, 12h, 24h, 48h and 72, n=10/ group). Animal model of EIU was established by a hind footpad injection of 200µg Cholera vibrio LPS in four groups (12h, 24h, 48h and 72) except 0h group (control group). Expression of TLR4, MyD88 and NF-ΚB p65 in iris ciliary body tissue was detected through immunohistochemical staining. Immunohistochemical localization of TLR4 and a resident tissue macrophage marker, cluster of differentiation 163 (CD163), was performed on whole mount isolated iris-ciliary body complexes. The distribution patterns and phenotypes of TLR4 and CD163 were further characterized by double-labeled immunofluorescence studies.

Results: : TLR4, MyD88 and NF-ΚB p65 were detectable in the iris stroma12 h after injection, and the number significantly increased 24, 48 h and decreased gradually 72 hours after injection (p<0.001 by one-way ANOVA). The morphology of these cells hardly changed 12-72 h after injection. CD163 was expressed in the uvea in all rats.During the inflammatory response phase (0-48 h after injection), the proportion of CD163 tissue macrophages having a round morphology increased concurrently with a decrease in the proportion of dendritiform CD163 cells (p<0.001 by one-way ANOVA). These changes occurred mainly in the macrophages located in the stroma bordering the iris endothelial layer. Double-labeling immunofluorescence demonstrated the co-expression of TLR4 and CD163 in round stroma cells with TLR4 located at the cell membrane and CD163 in the cytoplasm.

Conclusions: : The increased expression of TLR4 and its downstream signal transduction molecules MyD88, NF-ΚB p65 indicate the potential role of TLR4-MyD88 dependent pathway in the pathogenesis of acute anterior uveitis (AAU). This has significant implications for the understanding of ocular inflammation and for interpreting the potential role of Gram-negative bacteria in the pathogenesis of acute anterior uveitis.Key wordsEIU, TLR4, CD163,MyD88, NF-ΚB p65.

Keywords: uveitis-clinical/animal model • uvea • immunohistochemistry 
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