The role of leukotriene A4 hydrolase in dictating inflammation and remodelling in chronic lung diseases

Inflammation is important in fighting infection, but it must be efficiently resolved and appropriate reparative processes must be instigated. In chronic lung diseases (CLDs), such as asthma and chronic obstructive pulmonary disorder (COPD), the processes go wrong resulting in persistent inflammation, aberrant repair and pathological remodelling such as scar tissue and overzealous mucus production. We need to understand why these processes go wrong so we can find a treatment for CLDs. I have shown that the enzyme leukotriene A4 hydrolase (LTA4H) regulates the levels of two mediators (LTB4 and PGP) that are critical in regulating inflammation and repair. I believe that this pathway goes wrong in CLDs, often driven by genetic alterations or environmental insults such as cigarette smoke, resulting in pathology.

I will study the LTA4H pathway, particularly in patients with CLD, to understand when and why it goes wrong and if we can correct it with novel drugs that I have developed.

My findings will help develop new treatments for CLDs.