The Nelin Lab’s focus is on inflammatory lung injury and the mechanisms leading to lung diseases, particularly bronchopulmonary dysplasia (BPD). BPD is the most common co-morbidity of extremely preterm birth. To improve the outcomes of these children, pre-clinical and translational work is desperately needed to understand the mechanism underlying disease progression and lung healing. The pathogenesis of BPD is currently incompletely understood, but it is likely multi-factorial with a common pathway of innate immune signaling. The Nelin Lab is interested in identifying novel therapeutic targets to either prevent lung injury or to prevent lung injury from progressing to BPD. The ultimate goal of this research is to understand the pathophysiology of BPD and the disease course of established BPD to improve the long-term outcomes of these infants.
The Nelin Lab has identified components of the L-arginine-Nitric Oxide pathway that can be manipulated to prevent lung injury. Its team is currently interested in up-stream signaling molecules that lead to the cascade of lung injury and chronic changes in the lung. This includes the mitogen-activated protein kinases (MAPK) and their regulation by mitogen-activated protein kinases phosphatase-1 (MKP-1 or DUSP1).
The Nelin Lab is also interested in how damage-associated molecular patterns, particularly HMGB1, amplify and perpetuate inflammatory signaling leading to lung injury and BPD. Its team utilizes in vitro and in vivo techniques to study molecular mechanisms and examines biomarkers (both genetic and protein biomarkers) of the pathways of interest in translational studies in neonates.