Monash University researchers have identified a critical role for a protein known as G-CSF in chronic obstructive pulmonary disease (COPD), an incurable lung disease often referred to as emphysema.

COPD is the third most common cause of death worldwide, afflicting 29% of people over 75 in Australia and its incidence is increasing. It responds poorly to current therapies, which have remained largely unchanged for decades.

The multi-disciplinary research team, led by Associate Professor Margaret Hibbs from the Department of Immunology and Pathology, showed that lung disease and other disease comorbidities such as osteoporosis, heart disease and body wasting failed to develop in an experimental COPD model when G-CSF was “knocked out” genetically. They also demonstrated that G-CSF levels were elevated in the lungs of patients with COPD, suggesting it played a destructive role.

The research is the first to strongly implicate G-CSF as a promising new therapeutic target in the treatment of COPD and COPD comorbidities, Associate Professor Hibbs said. This was important because much of the suffering and health care burden inflicted by COPD is attributed to these co-existent diseases.

“Nothing has proved to be effective in treating patients with COPD so we’re now attempting to target this protein. This would be the first strategy to be discovered to treat the lungs and the comorbid diseases at the same time, which would be of huge international significance,” she said.

G-CSF is better known for its role as a ‘growth factor’ stimulating the production of white blood cells called neutrophils, which help the body fight infection, and it is used to boost production of these cells in cancer patients undergoing chemotherapy. These beneficial roles have overshadowed the exploration of the role of G-CSF in chronic inflammatory diseases.

“We were thinking that G-CSF was not only promoting the development and activity of neutrophils but was recruiting large numbers of other white blood cells to the lung,” Associate Professor Hibbs said. “We found that when G-CSF was eliminated we reduced white blood cells in the lungs and they no longer became diseased.” White blood cells help fight lung infections but when there are too many of them they can cause destructive lung disease through their production of enzymes and inflammatory factors.

The researchers are approaching a pharmaceutical company about making a biologic drug to target G-CSF and are extending their studies into the role of G-CSF to other lung diseases. The first author of the study was Dr Evelyn Tsantikos from Monash University. Associate Professor Hibbs worked closely on the study with long-term collaborator Professor Gary Anderson from the University of Melbourne.