Abstract
Purpose::
To examine how desiccating conditions following PRK affect the distribution of macrophages and dendritic cells in the stroma as well as inflammatory mediators and Arginase II (ASE).
Methods::
: Forty 4-8 week old female Balb/C mice were used in this study. Ten served as controls. Ten were placed in desiccating conditions (DE). The other twenty mice underwent bilateral corneal epithelial scraping using an electric brush prior to PRK and were divided in two additional groups: Ten mice were placed in normal conditions (NC) and the other ten mice were exposed to a DE for one week. Immunohistochemistry studies were performed using CD45, GR-1, CD11b, CD 11c, INF-γ, Cox-2, Arginase II, and alpha SMA antibodies
Results::
Increased numbers of leukocytes (CD-45+) were found in the stroma of eyes with epithelial injury that were subjected to DE. Significant increases (p<0.05) were found in CD11b+ (macrophages and dendritic cells) and GR-1 (neutroplils) cells in DE eyes with PRK in comparison to either DE or PRK alone. These changes were correlated with increased expression of COX-2 and Arginase II in the epithelium and stroma. INF-γ was expressed in DE but significantly increased in the stroma in DE eyes with PRK
Conclusions::
Our results suggest that elevated expression of ASE in mice after PRK and exposed to a desiccating environment may play a role in the healing response. This enzyme is involved in the production of ornithine, a precursor of collagen synthesis. It is possible that the monocytes use the Arginine-ornithine pathway to repair the damage caused by the inflammatory response after surgery. Manipulation of ASE activity or expression may affect the corneal wound healing response. Studies are underway using knock-out mice for ASE to determine its role in the corneal response.
Keywords: wound healing • cornea: tears/tear film/dry eye • refractive surgery: PRK