HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Ueta, M. Articles by Kinoshita, S. Search for Related Content PubMed PubMed Citation Articles by Ueta, M. Articles by Kinoshita, S.

Spontaneous Ocular Surface Inflammation and Goblet Cell Disappearance in IB Gene-Disrupted Mice

¹From the Department of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan; the ²Department of Host Defense and the ³Quarters for Experimentally Infected Animals, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.

PURPOSE. The ocular surface epithelium is part of the mucosal defense system. Because transcription factor NF-B 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-B, IB, in murine ocular surface inflammation.

METHODS. The eyes of IB^–/– mice were analyzed biomicroscopically and histologically. IB 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. IB mRNA on the ocular surface and in other mucosal tissues was localized by in situ hybridization.

RESULTS. IB^–/– mice manifested chronic inflammation, specifically in the ocular surface, but not in other tissues. In normal mice, IB was expressed in a variety of mucosal tissues. The IB transcript was predominantly distributed in the epithelia of these tissues. As inflammatory symptoms progressed on the ocular surface of IB^–/– 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 IB in the ocular surface epithelia negatively regulates the pathologic progression of ocular surface inflammation.

This article has been cited by other articles:

				M. Ueta, C. Sotozono, T. Inatomi, K. Kojima, K. Tashiro, J. Hamuro, and S. Kinoshita Toll-like receptor 3 gene polymorphisms in Japanese patients with Stevens-Johnson syndrome Br. J. Ophthalmol., July 1, 2007; 91(7): 962 - 965. [Abstract] [Full Text] [PDF]

				S. K. Swamynathan, J. P. Katz, K. H. Kaestner, R. Ashery-Padan, M. A. Crawford, and J. Piatigorsky Conditional Deletion of the Mouse Klf4 Gene Results in Corneal Epithelial Fragility, Stromal Edema, and Loss of Conjunctival Goblet Cells Mol. Cell. Biol., January 1, 2007; 27(1): 182 - 194. [Abstract] [Full Text] [PDF]