Objectives. Nitric oxide (NO) plays an important role as a signal molecule as well as a cytotoxic effector molecule of the nonspecific innate immune response. The aim of this study was to examine the role played by NO during P. aeruginosa keratitis.
Methods. In this study, we investigated the level of NO in BALB/c mouse eyes challenged with P. aeruginosa strains Pear1 (noninvasive/noncytotoxic), 6294 (invasive) and 6206 (cytotoxic). Following corneal challenge with P. aeruginosa, corneas were collected at 1, 8, 16, and 24 hours after infection. NO levels were measured by determining the nitrite and nitrate concentrations in the homogenates. Human corneal epithelial cells grown in tissue culture were also infected with P. aeruginosa strains and levels of NO measured.
Results. In the eyes infected with P. aeruginosa strain 6294, the level of NO peaked at 16 and declined at 24-hour after challenge. For Paer1, peak NO production was also noted at 16 hours after infection. Strain 6206 produced NO at maximal level from 8 to 24 hours. Human corneal epithelial cultures infected with P. aeruginosa showed no significant production of NO, indicating that the corneal epithelium is an unlikely source of NO during infection.
Conclusions. NO is produced during P. aeruginosa keratitis and may protect tissues from damage.
From the Institute for Eye Research, Vision CRC and School of Optometry and Vision Science, The University of New South Wales, Sydney NSW, Australia.
Address correspondence and reprint requests to Mark Willcox, PhD, School of Optometry and Vision Science, The University of New South Wales, Sydney NSW 2052, Australia; e-mail: email@example.com
Accepted August 29, 2007.