Our research is focused on understanding the molecular and cellular mechanisms that regulate innate immune responses during pneumonia and acute lung injury. We seek to define how immune cells coordinate antimicrobial defense while limiting excessive inflammation that contributes to lung tissue damage. Our broader goal is to identify novel therapeutic targets that promote the resolution of pulmonary inflammation and improve outcomes in patients with severe respiratory infections.

To achieve these goals, we investigate the signaling pathways and immune receptors that govern the function of alveolar macrophages, neutrophils, and other innate immune cell populations during bacterial and viral pneumonia. using molecular, cellular, and systems-level approaches, we examine how these pathways regulate inflammatory signaling, immune cell activation, and tissue repair to preserve lung functions throughout infection.

As part of our research program, we utilize clinically relavant mouse models of pneumonia, primary immune cell studies, Flow cytometry, transcriptomic analyses, and human clinical specimens to uncover mechanisms of host defense and identify new strategies for treating inflammatory lung disease.