The expression of intercellular adhesion molecule (ICAM-1) and vascular cell adhesion molecule (VCAM-1) were studied in the conjunctiva of diabetic patients with and without retinopathy. All patients underwent a complete ophthalmic examination including ocular fundus and retinal fluorescein angiography. The indirect immunoperoxidase method was performed on 15 normal conjunctivas taken during cataract surgery (group 1), on 40 eyes of 40 patients with type 2 diabetes without diabetic retinopathy (DR) (group 2) and 13 eyes of 13 patients with DR (group 3). ICAM-1 and VCAM-1 are located in epithelial cells, vascular endothelial cells and in stromal cells. Our results show a statistically significant increase in the immunohistochemical expression of these proteins in the conjunctiva of diabetic patients with and without DR in comparison with normal conjunctiva (P = 0.001). Noteworthy, ICAM-1 and VCAM-1 are upregulated in the conjunctiva of diabetic patients with and without retinopathy, reflecting the inflammatory nature of this condition and suggesting a possible role for these mediators in the pathogenesis of diabetic microangiopathy.

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The expression of apoptotic factors Bcl-2 and Bax were studied in the conjunctiva of diabetic patients with and without retinopathy. All patients underwent a complete ophthalmic examination including ocular fundus and retinal fluorescein angiography. The indirect immunoperoxidase method was performed on 15 normal conjunctiva taken during cataract surgery (group 1), on 40 eyes of 40 patients with type 2 diabetes without diabetic retinopathy (group 2) and 13 eyes of 13 patients with diabetic retinopathy (group 3). In normal human conjunctiva, Bax showed positive expression in epithelial, vascular and stromal cells whereas Bcl-2 staining was negative. In the conjunctiva of diabetic patients without diabetic retinopathy, Bax was widely, and strongly, expressed in epithelial cells, vascular endothelial cells, fibroblasts and infiltrating cells such as macrophages. For patients with diabetic retinopathy, Bax was consistently strong to very strong. Bcl-2 protein expression became weak to negative for diabetic patients both with and without diabetic retinopathy. Immunoreactivity was not correlated between Bcl-2 and Bax in the conjunctiva of diabetic patients. Bax was always localized in tissues characterized by a high rate of apoptosis, whereas, Bcl-2 was absent. Our results suggest that diabetic human conjunctiva, with its inflammatory phenomena, is considered as a privileged target for programmed cell death.

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