Expression of TLR4-MyD88 and NF-κB in the Iris during Endotoxin-Induced Uveitis. (3rd August 2010)

• Record Type: Journal Article
• Authors: Li, Shang; Lu, Hong; Hu, Xiaofeng; Chen, Wei; Xu, Yingzhi; Wang, Jing
• Other Names: Lepper Philipp M. Academic Editor.
• Is Part Of: Mediators of inflammation. Volume 2010(2010)
• Publication Date: 2010-08-03
• Subjects: Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1155/2010/748218
• Languages: English
• ISSNs: 0962-9351

Abstract

Abstract : Purpose . To observe the expression of Toll-like receptor-4 (TLR4), myeloid differentiation factor 88 (MyD88), and nuclear factor kappa B p65 (NF-κ 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 μ g Cholera vibrio LPS. Expression of TLR4, MyD88, and NF-κ 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 ( P < .001 ) 48 hours after injection, and decreased gradually 72 hours after injection. Expression of MyD88 and NF-κ B p65 is consistent with the change of the TLR4. Conclusions . The increased expression of TLR4 and its downstream signal transduction moleculesMyD88, NF-κ B p65 indicate the potential role of pathway in the pathogenesis of acute anterior uveitis (AAU).