It has been shown previously that particles ranging from 138 nm to 1.2 mm in diameter accumulated in the trabecular meshwork and demonstrated no correlation between the particle size and resistance to particle outflow, however these PD 173212 experiments did not examine 50 nm nanoparticles as we used here. We did not, however, find that magnetic microparticles led to an increase in IOP, suggesting that although they do not exit the eye efficiently, they did not clog the trabecular meshwork to a significant degree, possibly because of a difference in total number of particles injected. It has been shown that the injection of microbeads into the anterior chamber of rodents can be used to increase IOP and induce a rodent model of glaucoma. Using 15 mm particles, they found that the increase in IOP was due to microbead obstruction of the trabecular meshwork, not seen here with 4 mm particles. It is possible the more subtle forms of cytotoxicity before cell loss measured here could be detected with other modalities like specular or electron microscopy, and such studies may be warranted in the future. Japanese encephalitis is the cause of recurrent epidemic viral encephalitis in south-east Asia, with around 30,000�C50,000 cases reported every year resulting in 10,000 to 15,000 deaths. The JE virus is a positive sense single stranded RNA virus, with approximately 11 kb genome. JEV is a NU 9056 neuroptropic virus that causes extensive neuronal death, which is reportedly mediated by activating the tumor necrosis factor receptor -1 complex. One of the hallmarks of JEV infection is activation of microglia which is associated with increased cell-proliferation and bioactive/ inflammatory mediator production associated with distinct morphological changes. Although, certain activated glial-derived factors contribute to tissue repair, the interactive cross-talk between neuronal injury and microglial activation often determine the neuropathological outcome in JEV infection. The functional manifestations of such activated state are increased production of proinflammatory mediators like cyto/chemokines, reactive oxygen and nitrogen species by microglia. Increased release of proinflammatory mediators like tumor necrosis factor -a, IL-1b, IL-6, MCP-1 and RANTES have been observed from microglia activated by JEV infection. This release of cyto/chemokines represent the innate immune response against flaviviral infection of brain which in turn, is known to be mediated by the pattern recognition receptors such as toll like receptors and RIG-I�Clike receptors. RIG-I, a type of RLR, recognizes double-stranded RNA and uncapped 59 triphosphate RNA molecules, which are found in the genome of many RNA viruses or produced during viral replication.