Objective: To study the immunologic mechanism of corneal ulceration after alkali burn.
Methods: 55 rabbits with alkali burn in right eye were randomly divided into two groups. In group I (31 animals), the level of circulating immune complex (CIC), the rate of red blood cell C3b receptor complex rosette (RBC-C3bRR) and immune complex rosette (RBC-ICR) were measured respectively at 7, 14, 21, 35, 49 days after alkali burn. In Group 2 (24 animals), the immune complex was detected by means of immunofluorescence (IF) and immunogold-silver staining (IGSS) in burned tissues at 21 days after burn. Histopathologic changes were also observed under light microscope.
Results: CIC, the rate of RBC-C3bRR and RBC-ICR were markedly increased 14 to 21 days after burn. In the mean time, the deposition of immune complex was found in burned tissues and the accumulation of polymorphonuclear leukocyte (PMN) was observed at the base of corneal ulcer.
Conclusions: The immune mechanism indeed participates in the pathogenesis of corneal ulceration and also aggravates the progress of ulceration on the base of chemical injury.