We have studied the role of nitric oxide (NO) in two types of uveitis: (1) Anterior uveitis represented by the model of endotoxin-induced uveitis (EIU in the rat and (2) toxoplasma retinochoroiditis using a mouse model. In EI we have found NO levels that peak in the anterior chamber of the eye 2 hours before cellular infiltration and a sharp rise in protein exudation. Inhibition of NO production with a structural analog of L-arginine prevente the induction of EIU. In contrast, inhibiting NO synthesis during infectio with Toxoplasma gondii caused an exacerbation of the disease. Spleen cell cultures from infected mice produced a large amount of NO. NO production was associated with a reduced viability and proliferation of the lymphocyte to toxoplasma antigen. The lymphocyte proliferative response was restored by blocking NO production. In conclusion, it appears that NO has diverse, even opposing roles in uveitis, depending on the type and mechanism of the inflammatory process involved.
