Periostin deletion reduces corneal opacity and the infiltration of immune cells.

Corneal opacity resulting from corneal injury is a leading cause of blindness. The interaction of extracellular matrix (ECM) proteins, cytokines and immune cells induces corneal opacity after corneal injury. Periostin, which is secreted into the ECM, is involved in wound healing and is associated with immune cell infiltration. The function of periostin in corneal wound healing and in the development of corneal opacity was investigated. Wild-type (WT) and Postn knockout (KO) mice underwent central corneal incision. Periostin expression level was significantly increased after the incision in WT mice, correlating with higher levels of wound healing markers, such as fibronectin and α-SMA, and increased corneal opacity. However, Postn KO mice showed reduced corneal opacity and immune cell infiltration, particularly from myeloid lineage cells after incision. Additionally, pro-inflammatory cytokine levels (IL-1β, IL-6, C1q) were not significantly changed in Postn KO mice. The results suggest that periostin deletion impairs corneal wound healing and reduces opacity by regulating cytokine expression and immune cell recruitment. The findings indicate that periostin can be a potential therapeutic target for reducing corneal opacity.