Purpose: The etiologic mechanisms of bullous keratopathy (BK) after argon laser iridotomy (ALI) are still unknown. Therefore, we investigated potential mechanisms on BK after ALI.
Methods: Corneal endothelial surface obtained in penetrating keratoplasty for BK after ALI was observed and analyzed immunohistochemically. We investigated how various leukocytes react to cultured human corneal endothelial cells in an inflamed condition and monocytes/macrophages respond to the iris treated by an argon and YAG laser or pigmented and nonpigmented iris treated by an argon laser.
Results: We detected infiltration of CD68- and CD11b-positive monocytes/macrophages in the posterior surface of trephined corneas obtained during penetrating keratoplasty for BK after ALI in three of the seven eyes with ALI. In vitro, monocytes/macrophages, but not T cells, B cells, neutrophils, or pan-leukocytes, removed many cultured human corneal endothelial cells in the medium stimulated with proinflammatory cytokines. Human pigmented iris tissues treated by the argon laser, but not those treated by the YAG laser, attracted many monocytes/macrophages and formed large, round colonies. Human monocytes/macrophages formed large colonies on the argon laser-treated pigmented iris from C3H mice but not nonpigmented iris from albino BALB/c mice.
Conclusions: Our results suggest that monocytes/macrophages, argon laser, and pigmented iris are all involved in the pathogenesis of BK after LI.
Translational relevance: Etiology in BK after ALI has not been clear, but our findings based on clinical and experimental findings give a critical clue to explain possible mechanisms on BK after ALI.