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Mediators of Inflammation
Volume 2010 (2010), Article ID 748218, 7 pages
http://dx.doi.org/10.1155/2010/748218
Research Article

Expression of TLR4-MyD88 and NF- B in the Iris during Endotoxin-Induced Uveitis

1Departmnet of Ophthalmology, Beijing Chaoyang Hospital, Capital Medical University, No. 8 Baijiazhuang Road, Chaoyang District, Beijing 100020, China
2Department of Ophthalmology, Haidian Maternal and Child Health Hospital, Tonji Medical University, Beijing 100080, China

Received 25 November 2009; Accepted 21 June 2010

Academic Editor: Philipp M. Lepper

Copyright © 2010 Shang Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Purpose. To observe the expression of Toll-like receptor-4 (TLR4), myeloid differentiation factor 88 (MyD88), and nuclear factor kappa B p65 (NF- B p65) in iris tissue during endotoxin-induced uveitis (EIU) and evaluate the significance of these factors in uveitis. Methods.Wistar rats were randomly divided into 5 groups (0 h, 12 h, 24 h, 48 h, and 72 h, n = 10/group). Animal model of acute anterior uveitis was established by a hind footpad injection of 200  Cholera vibrio LPS. Expression of TLR4, MyD88, and NF- B p65 in iris ciliary body tissue was detected through immunohistochemical staining. Results. Expression of TLR4 was not detected in normal iris-ciliary body complex, TLR4 positive cells with round morphology appeared in the iris stroma 12 hours after injection, significantly increased 48 hours after injection, and decreased gradually 72 hours after injection. Expression of MyD88 and NF- B p65 is consistent with the change of the TLR4. Conclusions. The increased expression of TLR4 and its downstream signal transduction moleculesMyD88, NF- B p65 indicate the potential role of pathway in the pathogenesis of acute anterior uveitis (AAU).