The bacterium Pseudomonas aeruginosa (PA) is a leading cause of microbial infection of the cornea. One of the serious consequences of PA corneal infection is blindness resulting from persistent corneal inflammation. The innate immune system is the first line of defense against pathogens and is initiated by pattern recognition receptors which respond to invading microbes. It is known that IL-1β plays an important role in the induction of immune response in PA keratitis. In the classical immune response to bacterial infection, generation of mature IL-1β is a two-step process. The first step is the induction of pro-IL-1β expression, which is generally achieved by TLR-mediated activation of NF-κB pathway that results in the induction of pro-IL-1β. A second signal then triggers the assembly of inflammasomes leading to the cleavage of caspase-1. Active (cleaved) caspase-1 cleaves pro-IL-1β to generate active IL-1β, which is secreted from the cell to mediate downstream inflammatory effects that clear the infection. I am currently conducting studies to characterize the role of NLRP3 inflammasome in the clearance of P. aeruginosa infection of the cornea. In another study, we have made an exciting observation that galectin-8 knockout (Gal-8 KO) mice are resistant to PA infection. In an effort to understand the mechanisms that render Gal-8 KO mice resistant to PA keratitis, our working hypothesis is that Gal-8 has the capacity to dampen the activation of TLR pathway and/or inflammasome pathway. Overall goal of this project is to characterize the role of Gal-8 in the regulation of PA-induced immunopathology, and to develop effective strategies for prevention and regression of uncontrolled inflammatory response that results in extensive damage to the cornea and visual impairment.