Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 1996
Adhesion molecule expression in bullous keratopathy.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Zhu S N, Nölle B, Duncker G
Аннотация
BACKGROUND: Adhesion molecules may play an important role in the pathogenesis of bullous keratopathy.
METHODS: The expression of the integrin VLA-beta 1, alpha-subunits of the beta 2-integrins LFA-1, Mac-1, and p150,95, the members of the immunoglobulin family ICAM-1 and VCAM-1, and the selectin ELAM-1 on corneas with bullous keratopathy (BK) secondary to intraocular surgery was studied immunohistochemically using an APAAP method.
RESULTS: In the corneas with BK (in contrast to normal corneas), a downregulation of VLA-beta 1 was observed throughout the corneal tissues, particularly on the epithelial layer where bullae occurred; ICAM-1 was induced on epithelial membranes in both BK and inflamed corneas; and the expression of beta 2-integrins, VCAM-1 and ELAM-1 was upregulated in some specimens with remaining endothelial cells.
CONCLUSION: The results show that the investigated adhesion molecules may participate in the pathogenesis of BK. The decrease in VLA-beta 1 in patients with BK may be an important factor in the occurrence and development of recurrent bullae; the induced ICAM-1 may recruit beta 2-integrin-positive leukocytes into the epithelial layer, thus aggravating epithelial damage; and beta 2-integrins and VCAM-1 may play a role in endothelial injury and decompensation.
METHODS: The expression of the integrin VLA-beta 1, alpha-subunits of the beta 2-integrins LFA-1, Mac-1, and p150,95, the members of the immunoglobulin family ICAM-1 and VCAM-1, and the selectin ELAM-1 on corneas with bullous keratopathy (BK) secondary to intraocular surgery was studied immunohistochemically using an APAAP method.
RESULTS: In the corneas with BK (in contrast to normal corneas), a downregulation of VLA-beta 1 was observed throughout the corneal tissues, particularly on the epithelial layer where bullae occurred; ICAM-1 was induced on epithelial membranes in both BK and inflamed corneas; and the expression of beta 2-integrins, VCAM-1 and ELAM-1 was upregulated in some specimens with remaining endothelial cells.
CONCLUSION: The results show that the investigated adhesion molecules may participate in the pathogenesis of BK. The decrease in VLA-beta 1 in patients with BK may be an important factor in the occurrence and development of recurrent bullae; the induced ICAM-1 may recruit beta 2-integrin-positive leukocytes into the epithelial layer, thus aggravating epithelial damage; and beta 2-integrins and VCAM-1 may play a role in endothelial injury and decompensation.