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S.M. Nehls, M.T. Magone, E.C. Strauss; A MURINE MODEL OF CHRONIC SEVERE OCULAR ALLERGIC INFLAMMATION WITH FEATURES OF ATOPIC KERATOCONJUNCTIVITIS . Invest. Ophthalmol. Vis. Sci. 2004;45(13):4836.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Insights into the pathophysiology of acute allergic inflammation has been facilitated by studies using murine models that approximate human seasonal allergic conjunctivitis. However, investigations into the mechanisms mediating the severe and potentially blinding forms of chronic allergic disease have been restricted by the absence of a clinically relevant animal model. This study describes the development of a mouse model of severe, chronic ocular allergic inflammation with signs of atopic keratoconjunctivitis. Methods: Short ragweed pollen was used to sensitize and challenge SWR/J mice. The sensitization and challenge regimen was modified from a previous protocol (Strauss EC, et al, IOVS 1999, 40:1336–1342) to include repetitive immunizations over a 5 week period. Experimental groups were compared with control mice and analyzed for clinical, histological, and immunohistochemical features of chronic allergic inflammation. Results: Subsequent to ocular allergen challenge, mice developed clinical signs of severe, chronic allergic inflammation that included persistent lid edema, chemosis, and conjunctival injection. Moreover, peripheral neovascularization, superficial punctuate keratopathy, and anterior subcapsular cataracts were consistently observed. Tarsal papillary hypertrophy and sterile, central corneal ulcers were present in a subpopulation of experimental mice. Histology and immunohistochemistry studies revealed a cellular infiltrate consistent with chronic allergic inflammation. Conclusion: Chronic, severe allergic inflammation appears to be associated with repetitive allergen sensitization in mice with an atopic response predisposition. This new mouse model of chronic allergic inflammation, with findings suggestive of atopic keratoconjunctivitis, should facilitate investigations into the pathophysiology of severe ocular atopic disease. CR: none Support: NIH 1KO8EY014419
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