2006 Fiscal Year Final Research Report Summary
Role of corneal-conjunctival interaction on the pathogenesis of allergic conjunctivitis
Project/Area Number |
17591837
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Ophthalmology
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Research Institution | Yamaguchi University |
Principal Investigator |
KUMAGAI Naoki Yamaguchi University, Graduate School of Medicine, Associate Professor, 大学院医学系研究科, 助教授 (20234510)
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Co-Investigator(Kenkyū-buntansha) |
FUKUDA Ken Yamaguchi University, Hospital, Assistant Professor, 医学部附属病院, 講師 (70335751)
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Project Period (FY) |
2005 – 2006
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Keywords | allergic conjunctiva / cornea / chemokine / adhesion molecule / cytokine |
Research Abstract |
Recent studies have shown the correlation between the degree of corneal lesion and that of conjunctival inflammation in individuals with allergic conjunctivitis. It is also demonstrated by several researchers, including us, that corneal fibroblasts are the promoter of conjunctival inflammation through their potent release/expression of many cytokines, chemokines and adhesion molecules. In contrast, corneal epithelial cells are considered to be the quencher of conjunctival inflammation by their ability to separate corneal cells from bioactive substances in the tear fluids. In the current study, using rat experimental allergic conjunctivitis models, we examined the effect of corneal epithelial peeling on 1) clinical picture of conjunctivitis, 2)release/expression of cytokines, chemokines and adhesion molecules. We also examined 3) the effect of conjunctival allergic inflammation on the repair of corneal epithelium. Result 1) Corneal epithelial peeling enhanced the clinical picture of the late phase of allergic conjunctivitis. It also enhanced the number of eosinophils in the conjunctiva at the late phase. It had no effect on the early phase. 2) Corneal epithelial peeling enhanced the release/expression of chemokines TARC, RANTES, MCP-I and adhesion molecule ICAM-1 in the conjunctiva. It enhanced the release/expression of chemokines TARC, RANTES, IP-10, MCP-1 and adhesion molecule ICAM-1 and VCAM-1 in the cornea. 3) Induction of allergic conjunctivitis delayed the repair of corneal epithelium. Discussion In rat experimental allergic conjunctivitis model, corneal epithelium serves as a quencher of allergic inflammation. Corneal epithelial peeling enhances the late phase of allergic reaction possibly, at least in part, through the activation of structural cells of the cornea. Delayed epithelial repair of the cornea contribute the exacerbation of allergic inflammation in the conjunctiva.
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