We aim to understand the molecular mechanisms of host-pathogen interactions in the context of infections with gram positive bacteria, including Staphylococcus aureus and Listeria monocytogenes. We are particularly focused on investigating the mechanisms by which the host innate immune system restricts bacteria and the mechanisms by which pathogens subvert or evade these responses. These studies led to the discovery of a new host sensor of bacterial infection, the aldo-keto reductase AKR1C13, which we termed RECON. Using knockout mice, we have found that RECON is essential for the control of S. aureus and L. monocytogenes infection in vivo through the regulation of host inflammatory responses. Interestingly, in the absence of infection, Akr1c13 deficient mice display signs of liver disease as well as intestinal dysbiosis, likely as a result of chronic inflammation. Thus, we are interested in exploring both the roles of RECON in the control of bacterial infection as well as in the maintenance of liver and intestinal homeostasis using a combination of in vivo and ex vivo studies using organoid models. We ultimately hope that a more thorough understanding of the host processes regulated by RECON will pave the way for the design of new, immunomodulatory therapeutics for the treatment of infectious, malignant, and chronic inflammatory diseases.