Influence of interleukin-1α and tumor necrosis factor-α production on corneal graft survival

Aim To determine pro-inflammarory cytokine secretion from human corneas with different pathology and to establish whether cytokine profile influences corneal graft outcome. Method Secretion of both proinflammatory cytokine interleukin (IL)1 alpha and rumor necrosis factor (TNF)-alpha was measured after cultivation of 47 corneas collected from corneal graft recipients suffering from different corneal diseases. Non-inflammatory corneal diseases were keratoconus (n = 8), keratoglobus (n = 2), bullous keratopathy (n = 11), and Groenouw stromal dystrophy type 11 (n = 2), whereas inflammatory included vascularized corneal scar (n = 14), rejected graft (n = 6), and corneal ulcer (n = 4). Corneas were cultivated at 37 degrees C for 24 hours and frozen until cyrokine detection was measured by immunoassay. Donor corneas unsuitable for transplantation were used as controls (n = 7). Corneal graft recipients were followed at least 18 months and rejection race was calculated for each group. Results The median concentration of IL-1 alpha secreted from corneas of recipients with non-inflammatory diseases was 2.47 pg/mm(3) (range, 0.13-9.95). In inflammatory corneal diseases, IL-1 alpha concentration was significantly higher (median, 5.92 pg/mm(3); range, 0.48-12.68; P = 0.005). 11-1 alpha production in controls (median, 0.63 pg/mm(3); range, 0.36-1.29 pg/mm(3)) was significantly lower than in inflammatory corneal diseases (P < 0.001) and non-inflammatory diseases (P = 0.008). Low level of TNF-alpha was detected only in 5 cases of vascularized corneal scars, 3 cases of bullous keratopathy, and 3 cases of graph rejection. Rejection race was significantly higher in inflammatory than in non-inflammatory group (46036 vs < 10%, respectively, P = 0.008). IL-1 alpha and TNF-alpha were absent from all patient's sera, confirming its local intra-ocular production. Conclusion Increased production of IL-1 alpha in corneal recipients with inflammatory diseases suggests its role in corneal graft rejection in humans.