A role for GPR84 in inflammation-associated kidney injury
Co-Applicant(s): Baptiste Lacoste, Dylan Burger, William Stanford
Lay Abstract
Testing a new target to reduce inflammation and damage in kidney disease Inflammation can flare up in the filters of the kidney leading to leakage of protein from the blood into the urine. This inflammation is often associated with infections that result in sepsis or from autoimmune conditions where antibodies target the cells of the kidney’s filters. This process occurs quickly as white blood cells called neutrophils arrive in the filters to drive injury progression. There currently are very limited options for treatment of these types of inflammatory diseases. My lab wishes to address this unmet need. We are studying a cell surface receptor that is found on neutrophils, called GPR84 whose levels increase dramatically in a mouse model of sepsis-like kidney injury. Similarly, human patients with sepsis associated kidney disease also exhibit high levels of GPR84 in their kidneys. We now wish to test whether this increase in GPR84 expression either contributes to or helps to resolve the inflammation of the kidney’s filters. Our lab is equipped with a mouse line that has genetic deletion of GPR84, as well as drugs that either activate or block GPR84. An improved understanding of the role of this receptor on neutrophils during inflammatory kidney disease could help in developing more precise treatment options.
