Our lab develops integrated empirical and theoretical models of biological systems on various scales ranging from metabolic networks, gene networks and signal transduction models to multicellular models. We model individual cells (bacteria and mammalian) to study metabolic and genetic responses of E.coli., M. tuberculosis and macrophages to study changes in their environment. We also model interactions between cells (microbial and host-microbe) to understand the impact of exogenous stressors, host-induced stress, deficiencies and comorbidities on microbial communities and host-pathogen interactions. My current research project involves expanding an existing in-silico macrophage immune response model that captures the dynamics of the complex intracellular signaling pathways activated in response to Mycobacterium tuberculosis (Mtb) infection leading to production of inflammatory cytokines and effector molecules. Using a model based on ordinary differential equations (ODEs), we aim to examine the role of vitamin D3 in the regulation of these cytokines and effector molecules, and the ramifications of combined vitamin D3 deficiency and comorbid conditions (e.g., chronic alcohol consumption) on efficacy of the host innate immune response during infection and tuberculosis disease.