1. ¹Cooperative Research Centre for Eye Research and Technology, School of Optometry, University of New South Wales, Sydney, New South Wales, Australia
2. ²Department of Veterinary Anatomy and Pathology, University of Sydney, Sydney, New South Wales, Australia

Correspondence: Dr Mark Willcox, CRCERT, University of New South Wales, Sydney, NSW 2052, Australia. Email: m.willcox@cclru.unsw.edu.au

Received 15 June 1999; Accepted 26 July 1999.

Abstract

Pseudomonas aeruginosa can cause ulcerative bacterial keratitis. A feature of keratitis is the rapid infiltration of the avascular corneal stroma by neutrophils. KC is a potent neutrophil chemokine. The present study used a mouse model of ocular infection to assess the relationship between KC and inflammation in the cornea in response to challenge with a strain of P. aeruginosa causing keratitis. Low levels of KC mRNA and protein were detected by in situ hybridization and ELISA, respectively, in unchallenged corneas. Dramatically increased numbers of KC mRNA⁺ cells were present in P. aeruginosa strain 6294-challenged corneas. Expression of KC mRNA was found to be up-regulated in the corneal epithelium in response to wounding alone. The KC mRNA⁺ cells were located in the epithelium and corresponding to infiltrating neutrophils cells in the stroma. Quantification of KC protein at different time points showed peak levels at 8 h of bacterial challenge. These results suggest that KC may be involved with the regulation of leucocyte infiltration early during bacterial keratitis.