Their results, which also confirmed this novel pathway may contribute to lung damage in adult patients with cystic fibrosis (CF), are being published in the July issue of The Journal of Immunology.
Jay K. Kolls, MD, who is the division chief of Pediatric Pulmonology, Laboratory of Lung Immunology and Host Defense at Children's Hospital of Pittsburgh, and professor of Pediatrics and Immunology at the University of Pittsburgh School of Medicine, and his research team measured mediators of inflammation in cystic fibrosis patients, focusing on interleukin 23 (IL-23) and interleukin-17 (IL-17).
"The results show that IL-23 and IL-17 may be good targets for neutralization and blocking the inflammatory response," said Dr. Kolls adding that "this research shows us that with the newly identified pathway of inflammation, it may be possible to treat the patient earlier and more effectively, which could prevent lung disease or give patients a better quality of life and longer lifespan."
Dr. Kolls added, "What's intriguing is that by targeting IL-17 we may also be able to inhibit IL-8, a well-known inflammatory instigator in CF, since our laboratory studies suggest expression of this cytokine is dependant on IL-17. A treatment that focuses on IL-17 instead of IL-8 may be the more rational approach."
Because in CF patients the inflammation is never "shut off" and infections cannot be resolved, researchers have been looking for other ways to treat the inflammation associated with the disease. Throughout most of the world, lung infections are a major cause of death and illness among children. Although death rates are low in the United States,
Contact: Melanie Finnigan
Children's Hospital of Pittsburgh