Our laboratory explores the interaction of bacterial pathogens with host cells, focusing on how mammalian cellular stress signaling sculpts transcriptional, spatial and metabolic reprogramming during the innate immune response.

Innate immune signaling and inflammation are foundations for effective host defense against microbial infection. Dysregulation of these responses can drive pathological immune responses that lead to autoimmunity and chronic inflammatory disease. Cellular perturbation by infection or other kinds of stress elicit specific signaling pathways, termed cellular stress responses, triggered by sensors of endoplasmic reticulum unfolded proteins (unfolded protein response; UPR), nutrient stress (integrated stress response; ISR) and mitochondrial stress. We study mechanisms by which these stress response pathways synergize with innate immune signaling to regulate specific inflammatory responses. Using different bacterial pathogens, including methicillin-resistant Staphylococcus aureus, Listeria monocytogenes and Salmonella enterica, we are investigating how macrophages, neutrophils and epithelial cells alter subcellular structure and organization to enable robust inflammatory responses, anti-microbial defenses, metabolic remodeling, survival, and differentiation.