Research Area C: Inflammation in Aging-associated Diseases

Inflammation is now recognized as a critical player in the pathogenesis of multiple human diseases and as an important risk factor for cancer development. The contribution of chronic inflammation to aging-associated diseases has recently gained increasing attention by providing a link between dietary inputs, metabolic processes, cellular stress responses, innate immunity, and tissue damage. However, the mechanisms that control inflammatory responses and govern disease onset and progression remain unclear. A complex network of soluble mediators such as TNF, IL-1, IL-6, and other potent cytokines, regulates inflammatory responses by activating distinct intracellular signaling cascades, including the NF-kappaB and mitogen-activated protein kinase (MAPK) pathways, on both immune and non-immune cells.
The aim of research area C is to elucidate the cellular and molecular mechanisms controlling inflammation at the interface of innate immunity, metabolic processes, and cellular stress responses, and affecting the pathogenesis of chronic aging-associated diseases, with particular focus on atherosclerosis, type 2 diabetes mellitus and inflammation-associated cancer. Using the mouse as the primary experimental model, a large number of conditional mutants will be employed to dissect in vivo the function of inflammatory mediators and signaling pathways in disease pathogenesis.
In parallel, human genetics studies will be performed to identify genetic loci associated with susceptibility to chronic inflammatory diseases as a prelude to evaluating candidate genes in the mouse model.

Coordinator:

Prof. Dr. Manolis Pasparakis,
Institut für Genetik
 
email: pasparakis(at)uni-koeln(dot)de