Dry eye predisposes to corneal neovascularization and lymphangiogenesis after corneal injury in a murine model.

Dry eye disease is becoming recognized as an immune-inflammation mediated disorder. Surgical insults such as corneal incision or suture can aggravate dry eye. We sought to determine whether underlying dry eye aggravates corneal inflammatory infiltration, hemangiogenesis, and lymphangiogenesis (LY) induced by surgical injury in a murine model. We used treatment arms; one, normal eye (non-dry eye) and the other, a scopolamine-induced dry eye model. We first compared the corneas of both groups on which no surgery was performed with confocal and fluorescent microscopy. In subgroups of each treatment arm, we made a corneal incision followed by 2 corneal sutures to approximate the wound. After harvesting the cornea on postoperative day 9 and immunohistochemical staining, we compared corneal neovascularization (NV), LY, and CD11b inflammatory cell infiltration between non-dry eye and dry eye groups. In corneas in which no surgery was performed, the dry eye group showed more CD11b cell infiltration than did the non-dry eye group (P < 0.05). With respect to corneas after injury, there was significantly more hemangiogenesis, LY, and inflammatory infiltration in the dry eye group than in the non-dry eye group (all P < 0.05). The underlying status of the cornea, whether it is dry or not, plays a significant role in the development of NV, LY, and inflammation after corneal injury. Dry eye can aggravate post-injury NV, LY, and inflammation.