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Published on: September 12, 2014
Therapeutic effect of amniotic membrane in persistent epithelial defects and corneal ulcers in herpetic keratitis
Natasa Brijacak1, Iva Dekaris, Alenka Gagro
1Department of Ophthalmology, General Hospital Virovitica, Virovitica, Croatia.
Amniotic membrane transplantation (AMT) promotes rapid epithelialization and reduces stromal inflammation and ulceration in HSV-1 keratitis. 18 patients with non-healing epithelial defect or corneal ulcer caused by herpetic keratitis were included in the study. All patients were treated by AMT. Corneal epithelial cells in patients suffering from herpetic keratitis secreted 5+/-4.8 pg/ml of IL-1alpha and 0.16+/-0.47 pg/ml of IL-1beta (mean+/-SD). IL-1alpha level was significantly higher as compared to controls (p<0.005). Amniotic membranes that were used to treat investigated patients contained 339.87+/-105 pg/ml of IL-1ra. In herpetic keratitis pro-inflammatory cytokine IL-1alpha is secreted from corneal epithelial cells in significantly higher level then in controls. Beneficial effect of the AMT in such patients could be explained by the fact that AM secretes its natural antagonist IL-1ra.
Amniotic membrane transplantation (AMT) promotes rapid epithelialization and reduces stromal inflammation and ulceration in HSV-1 keratitis. 18 patients with non-healing epithelial defect or corneal ulcer caused by herpetic keratitis were included in the study. All patients were treated by AMT. Corneal epithelial cells in patients suffering from herpetic keratitis secreted 5+/-4.8 pg/ml of IL-1alpha and 0.16+/-0.47 pg/ml of IL-1beta (mean+/-SD). IL-1alpha level was significantly higher as compared to controls (p<0.005). Amniotic membranes that were used to treat investigated patients contained 339.87+/-105 pg/ml of IL-1ra. In herpetic keratitis pro-inflammatory cytokine IL-1alpha is secreted from corneal epithelial cells in significantly higher level then in controls. Beneficial effect of the AMT in such patients could be explained by the fact that AM secretes its natural antagonist IL-1ra.
