Figure 3.

Deletion of a LXA₄ biosynthetic pathway or topical treatment with LXA₄ regulates PMN recruitment to the injured cornea. A: PMN content of corneas from 12/15-LOX KO mice and matched congenic wild-type (wt) controls was assessed by measuring tissue MPO activity after 7 days of chronic injury (n = 4, P < 0.02). A MPO calibration curve was established with inflammatory exudate peritoneal PMN and used to calculate relative tissue PMN numbers. B: 15-HETE formation, a metabolic precursor for LXA₄ formation, was determined by LC/MS/MS-based lipidomic analyses after 4 days of chronic injury (n = 4; *P < 0.05). C: Topical action of LXA₄ on PMN recruitment to the injured cornea was determined at 48 hours. Relative PMN numbers in uninjured corneas and injured corneas treated with either saline alone or LXA₄ (100 ng, t.i.d.) were assessed by measuring total tissue MPO activity (n = 4, *P < 0.02).