REACTIVE INFLAMMATION AND NEOVASCULARIZATION – KEY MECHANISMS OF CORNEAL OPACITY IN CHEMICAL ALKALINE BURNS
DOI:
https://doi.org/10.11603/2414-4533.2026.1.16103Keywords:
alkaline corneal burn in an experiment, reactive inflammation, cellular and humoral immunity, neovascularizationAbstract
The aim of the work: To investigate the main mechanisms and dynamics of reactive inflammation and their effect on angiogenesis in eye tissue during chemical alkali burns of the rabbit cornea in experiment.
Materials and Methods. The corneal damage model was reproduced in two rabbits groups: control – 10 intact animals and experimental – 10 animals, with simulated chemical burn of the cornea with alkali. The material was collected on the 1st, 7th, 14th and 21st days, that was based on the stages of the burn process in the corneal tissue. The activity of the inflammatory process was assessed by the dynamic of indicators of cellular and humoral immunity using generally accepted methods. The degree of corneal neovascularization was determined with an ophthalmoscope using the Efron scale.
Results. Clinical signs of the reactive inflammatory process with dystrophic-necrotic changes of the cornea in rabbits with corneal burn injury by alkali develop in the acute period. At the same time reparative processes are activated in the damaged eye, which leads to partial restoration of the epithelial cover, subsidence of stromal edema, and stimulation of angioneogenic processes in the cornea and loss of its transparency. Alkaline burn of the cornea was accompanied by intensification of cellular and humoral factors of immune defense, excessive production of pro-inflammatory cytokines, which are potential stimulators of the development of pathological angiogenesis - neovascularization. The development of new branched and fragile vessels in the corneal tissues is accompanied by active tissue remodeling and fibrosis. Neovascularization leads to persistent inflammation, scar formation, which threatens corneal transparency disorders.
Conclusions. Clinical signs of the reactive inflammatory process develop with dystrophic-necrotic changes of the cornea in acute period of experimental chemical burn of the cornea with alkali. It is manifested by damage to the epithelium with the formation of persistent epithelial-stromal defects (PESD) and initial manifestations of neovascularization. A pronounced staged activity of the inflammatory process is observed at the same time. The functional activity of neutrophils in the stimulated nitroblue tetrazolium test (sNST) is significantly increases, the reserve index and the coefficient of metabolic activation of neutrophils are significantly decrease. The predominance of the T-helpers growth over the level of cytotoxic T-lymphocytes, suppression of immunoglobulin secretion, a significant increase in the level of Circulating Immune Complexes and the concentration of pro-inflammatory cytokines become a trigger for angioneogenesis in the cornea, its neovascularization and loss of transparency.
Received: 09.01.2026 | Revised: 03.02.2026 | Accepted: 23.02.2026
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