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M. Ueta, J. Hamuro, E. Ueda, M. Yamamoto, S. Akira, S. Kinoshita; Spontaneous Ocular Surface Inflammation in IkappaBzeta Gene–Disrupted Mice . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4532.
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We previously reported that IΚBζ–/– mice manifested chronic inflammation, specifically in the ocular surface. We manipulated IΚBζ–/– mice to be Balb/c background. In this study, we analyzed Balb/c background IΚBζ–/– mice to elucidate the pathophysiology of the inflammation more clearly.
The eyes and skin of Balb/c background IΚBζ–/– mice were biomicroscopically and histologically analyzed.
While no IΚBζ+/+ and IΚBζ+/– mice exhibited symptoms of ocular surface inflammation throughout the experimental period (until they reached the age of 32 weeks), IΚBζ–/– mice became spontaneously symptomatic by 6 weeks. Redness and swelling of perioral and neck skin was observed following ocular surface inflammation. Histological analysis of the eyes and prioral skin of IΚBζ–/– mice aged 13 weeks showed heavy infiltration by inflammatory cells into the submucosal area of the conjunctiva and dermis. Moreover, we noted degeneration and loss of goblet cells in the conjunctival epithelia of both the palpebral and bulbar conjunctiva. Neither obvious pathological changes nor infiltrated inflammatory cells were detected in the eyes and skin of IΚBζ+/– mice of the same age.
We postulate that IΚBζ in the ocular surface epithelia negatively regulates the pathological progression of ocular surface inflammation.
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