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Mayumi Ueta, Junji Hamuro, Masahiro Yamamoto, Kazuhiro Kaseda, Shizuo Akira, Shigeru Kinoshita; Spontaneous Ocular Surface Inflammation and Goblet Cell Disappearance in IκBζ Gene-Disrupted Mice. Invest. Ophthalmol. Vis. Sci. 2005;46(2):579-588. doi: 10.1167/iovs.04-1055.
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purpose. The ocular surface epithelium is part of the mucosal defense system. Because transcription factor NF-κB in mucosal epithelial cells plays a central role in regulating the genes that govern the onset of mucosal inflammatory responses, we examined the role of a regulator of NF-κB, IκBζ, in murine ocular surface inflammation.
methods. The eyes of IκBζ−/− mice were analyzed biomicroscopically and histologically. IκBζ expression in normal mouse cornea and conjunctiva was examined by RT-PCR. The results were compared with those obtained in other tissues by real-time PCR. IκBζ mRNA on the ocular surface and in other mucosal tissues was localized by in situ hybridization.
results. IκBζ−/− mice manifested chronic inflammation, specifically in the ocular surface, but not in other tissues. In normal mice, IκBζ was expressed in a variety of mucosal tissues. The IκBζ transcript was predominantly distributed in the epithelia of these tissues. As inflammatory symptoms progressed on the ocular surface of IκBζ−/− mice, inflammatory cells, mainly CD45R/B220+ and CD4+ cells, intensely infiltrated the submucosa of the conjunctival epithelia. This infiltration was accompanied by an almost complete loss of goblet cells in the conjunctival epithelia.
conclusions. The authors postulate that IκBζ in the ocular surface epithelia negatively regulates the pathologic progression of ocular surface inflammation.
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