The role of arachidonic acid metabolites in the mediation of the polymorphonuclear leukocyte response following corneal injury.

The immediate polymorphonuclear leukocyte (PMN) response in the tear fluid was investigated following five different types of corneal injury. All injuries produced significant amounts of PMNs in the tear fluid within the first 6 hr of injury. Histological examination of injured corneas demonstrated that PMNs were attached to the denuded surface but were unable to attach to intact epithelium. Topical arachidonic acid, prostaglandin (PG) PGE1 and PGE2, and prostacyclin (PGI2) induced the arrival of PMNs into the tear fluid of normal rabbit eyes, but topical PGF2 alpha, PG-6-keto-PGF1 alpha, and thromboxane did not elicit a PMN response from normal conjunctiva. Tear fluid samples 2 to 4 hr following corneal epithelial denudation demonstrated PGE-type activity. Pretreatment with topical (0.05% and 0.5%) and intraperitoneal (i.p.) indomethacin (100 mg/kg) markedly inhibited the PMN response following partial corneal epithelial denudation. However, an i.p. dose of 5 mg/kg indomethacin potentiated the tear fluid PMN response following corneal injury. The inhibition of the PMN response by indomethacin suggested that arachidonic acid metabolites may be involved in the mediation of PMN chemotaxis following corneal injury.