Research
Iron handling and Alveolar Macrophage Function and Metabolism
We wish to understand how iron metabolism pathways regulate normal and pathogenic responses of lung alveolar macrophages (AMs) to infection and injury, and how this impacts COPD. AMs are the critical drivers of persistent inflammation in COPD, yet little is known about how AMs are dysregulated, why they persist in the lung for many years and why current treatments for COPD fail to modulate their activity. Our research focuses on investigating how disturbances in iron metabolism underlie and drive alveolar macrophage-associated immune system disarray in COPD. We are interested in iron uptake, turnover, metabolism and export in alveolar macrophages and how these normal homeostatic processes are essential for the innate immune response to infection.
Regulation of Mitochondrial Iron by Mitoferrins
Our lab is interested in how iron is transported into and out of the mitochondrion. SLC25A28 (mitoferrin-2) and SLC25A37 (mitoferrin 1) are inner mitochondrial membrane proteins that are thought to be involved in iron transport across the mitochondrial inner membrane into the mitochondrial matrix. We wish to examine how these transporters contribute to normal mitochondrial function, metabolism and dynamics in the cell and how they co-ordinate with other aspects of cellular iron regulation.
Iron Overload in COPD
As the fourth leading cause of mortality worldwide, Chronic Obstructive Pulmonary Disease (COPD) remains an incurable, inflammatory lung disease that is hard to diagnose early and has few therapeutic treatment options. Work from our laboratory has identified that iron metabolism pathways are dysregulated in the lungs of COPD patients and that targeting these pathways may hold promise for the development of new therapies for COPD. We wish to decipher where in the lung this iron accumulates and how this excess of iron affects the pathogenesis of the disease. We are asking the questions;Where does this iron come from; given cigarette smoke contains very little iron? What cells types are important in iron accumulation in the lung?Will having more iron promote the growth of bad bacteria rendering COPD patients more susceptible to infection?
