Inhibition of nitric oxide production exacerbates chronic ocular toxoplasmosis

There is considerable controversy, as to the roles of parasite proliferatio n and the inflammatory response in destruction of the retina during Toxopla sma gondii infection. A murine model was used to investigate the role of ni tric oxide in pathogenesis of chronic ocular toxoplasmosis. Increased quant ities of messenger RNA (mRNA) transcripts for iNOS were detected in the eye s of chronically infected C57BL/6 mice compared with noninfected control mi ce. Inhibition of nitric oxide (NO) by the addition of L omega-nitro-L-argi nine methyl ester (L-NAME) to the drinking water of infected mice between w eeks 4-6 of infection, exacerbated ocular inflammation. The amount of infla mmation was assessed semiquantitatively in-histological sections of the eye . Eyes from L-NAME treated mice showed a significant increase in inflammati on of the retina (P = 0.02), choroid (P = 0.03), and vitreous (P = 0.02) co mpared with control mice. These results demonstrate a protective role for N O in the control of chronic, ocular toxoplasmosis.