Acute inflammation is the body’s response to infection or injury; the inflammatory response regulates the recruitment of cells from the blood to kill invading microorganisms and promote wound healing. Normally this response resolves within a few hours or days, however chronic inflammation can cause disease including arthritis, atherosclerosis and even cancer.
Our group is interested in the normal mechanisms that mediate the resolution of inflammation and how these may be disregulated in chronic inflammatory diseases. We are also investigating how pathogens and cancer cells manipulate endogenous anti-inflammatory mechanisms to evade detection and elimination by the immune system.
We have a specific interest in cell signalling pathways that regulate myeloid cell phenotype and function in inflammation and cancer. We discovered the transcription factor; nuclear factor-κB (NF-κB), has a critical role in the resolution of inflammation by inhibiting macrophage activation in infection and cancer, our further studies have shown that cancer cells a pathogens promote activation of NF-κB to evade the immune response.
Our current research is focussed on further characterisation of how signalling pathways are manipulated by pathogens and cancer cells to evade of host immunity and what may be the molecular targets to increase host immunity to infection and cancer. These mechanisms may also be disregulated in chronic inflammatory and autoimmune diseases and could represent therapeutic targets.