Inflammation mediated by pattern recognition receptors (PRRs) is an important determinant in altering the risk of many chronic diseases. PRRs activate inflammatory responses by recognizing pathogen-derived molecules or endogenous damage-associated molecules (DAMPs). Most DAMPs are released from dying cells, tumour cells and injured tissue, and include degraded extracellular matrix components, heat-shock proteins, and nucleic acids. Evidence strongly suggests that excessive or protracted PRR signalling is central to the pathogenesis of chronic inflammatory diseases such as preeclampsia and cardiovascular diseases, diabetes, inflammatory bowel disease and rheumatic diseases.
By conducting studies on specimens from various clinical cohorts, we will explore how genetic determinants of the host response, gene expression patterns and cellular responses are associated with patient characteristics, prognosis of disease and response to treatment. Our studies will aim to give a critical reappraisal of pathogenetic mechanisms in chronic inflammatory disorders, as well as to provide a basis for the development of novel therapeutic and diagnostic modalities for these diseases.
This theme has three focus areas:
- PRR ligands and signalling in preeclampsia and cardiovascular disease
- PRR ligands and signalling in inflammatory bowel disease
- PRR ligands and signalling as underlying mechanism for bone destruction