Inflammation is a protective response to noxious stimuli that originate from infections and injured tissues. The inflammatory process triggered in response to microbial infections is instigated by pathogen-associated molecular patterns (PAMPs), while the one elicited by tissue damage is initiated by the release of danger-associated molecular patterns (DAMPs). PAMPs and DAMPs are both recognized by pattern recognition receptors (PRRs), and each generates a signaling cascade that in turn regulates the development and potency of the inflammatory process, increases vascular permeability, and recruits immune cells to the site of injury or infection. Under physiological conditions, inflammation is characterized by an initial destructive phase, followed by a reparative phase that restores tissue homeostasis. Conditions that perturb the balance between the destructive and reparative phases may lead to inflammatory disorders, including (but not limited to) autoimmune disease and cancer.
The Zanoni lab seeks to understand the events that initiate protective immunity in response to infection and tissue injury, or that drive the development of immune-mediated diseases; to this end, we scrutinize innate immune cell biology, with a primary focus on unraveling the PRR signaling pathways that are triggered by PAMP and DAMP encounter. The organizing principles that govern PRR signaling are largely unknown. We believe that elucidation of these principles will answer fundamental questions about the pathophysiology of the inflammatory process. Our current strategy for achieving these goals is to integrate findings derived from a combination of in vitro signaling studies and in vivo murine models, apply this information to refine our hypotheses, and create models that can explain - and possibly predict - the pathophysiology of inflammation in humans.