NF-KB and IL-17 dependent immune mechanisms in the development of chronic respiratory diseases

• Applicant: Professor Dr. Christoph Beisswenger
• Subject Area: Pneumology, Thoracic Surgery
• Term: from 2011 to 2016
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 203084958

Lung emphysema and chronic bronchitis are hallmarks of the Chronic Obstructive Pulmonary Disease (COPD). Studies from our lab and others suggest that factors of the innate immune system, such as the NF-κB signaling cascade, play a role in the development of smoke induced lung injury. Furthermore, it has been shown that factors of the adaptive immune system (e.g. Th-17 cells, IL-17, and IL-22) that are important for the clearance of infections are increased in the lungs of COPD patients. It is the aim of this project to examine the innate and adaptive immune mechanisms contributing to the development of chronic lung diseases, such as COPD. It will be examined whether Th-17 cells and the NF-κB signaling cascade play a role in the development of lung injuries and whether the inflammatory mediators IL-17 and IL-22 contribute to tissue destruction, emphysema, and loss of lung function. The role of the transcription factor NF-κB as well as the inflammatory mediators IL-17 and IL-22 in the development of lung injuries will be studied with the help of mouse models in which myeloid NF-κB signaling is differentiated from epithelial NF-κB signaling. The cellular mechanisms leading to tissue destruction will be studied with the help of human primary tissue culture experiments. This project will result in new biological findings regarding the development of COPD and will offer new approaches for therapies.

• DFG Programme: Research Grants