Regulation of inflammatory responses in vivo
Inflammation is the response of vascularised tissues to injury, metabolic disturbance and infection. Acute inflammation typically lasts only a few days while chronic inflammation can last for months or years, and is a defining feature of many important human diseases including rheumatoid arthritis and coronary heart disease.
The Greaves Laboratory is studying the role played by a family of inflammatory mediators called chemokines in the recruitment and activation of monocytes and macrophages during chronic inflammation. We are interested in the role chemokines play in atherosclerosis - a disease process that occurs in arteries causing angina, heart attacks, strokes and peripheral arterial disease.
In recent experiments, we showed that lipoprotein ApoA1 significantly down-regulates monocyte/macrophage responses to a wide range of inflammatory chemoattractants in vivo and in vitro.
Current work in the laboratory seeks too identify molecules that can regulate the efficiency of macrophage phagocytosis of both microrganisms such as bacteria and apoptotic neutrophils a process called efferocytosis.
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