Safer Agents for Chemical Reductions

Their findings were reported in the July 2005 issue of The Journal of Immunology.

The 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,” noted Dr. Jay R. Kolls, division chief of pediatric pulmonology, Laboratory of Lung Immunology and Host Defense, Children's Hospital of Pittsburgh (PA, USA).

Dr. Kolls added, "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.”
Targeting IL-17 may also inhibit IL-8, a well-known inflammatory instigator in CF, according to Dr. Kolls. "Laboratory studies suggest expression of IL-8 is dependant on IL-17. A treatment that focuses on IL-17 instead of IL-8 may be the more rational approach.”

Lung infection is the leading reason why children with CF visit doctors. Although clinical trials of nonspecific anti-inflammatory therapies have shown clinical benefit, significant side effects have limited their usefulness. "This work identifies a target for more specific regulation of the inflammatory pathways that ultimately contribute to lung damage in CF,” observed co-author Joseph Pilewski, M.D., associate professor of medicine at the University of Pittsburgh School of Medicine (PA, USA). "Modulating this pathway could lead to a safer and more effective anti-inflammatory therapy for CF and perhaps other inflammatory lung diseases.”