A passionate and inspired scientist, Dr Christina Bursill has led the Immunobiology since its formation in 2013.
The Immunobiology Group is a tightly knit group composed of one post-doctoral researcher, three PhD students, one research assistant, an honours student and a Marcus Blackmore Fellow, Dr Stacey Robinson from the HRI UK. Christina enthuses about her team at the HRI, “We have a group of high quality scientists who work well together,” Christina explained. “We are supported by great leaders and we maintain close collaborative links with the universities and hospitals.”
Christina finds her work both challenging and immensely rewarding. “I love coming up with new ideas, implementing them and seeing what results we get,” said Christina. “It thrills me to develop students over time, seeing their progress and growth, and of course I love the exchange of ideas when meeting other scientists at conferences.”
The group’s overarching purpose is to investigate the role of HDL, often referred to as the “good cholesterol” and inflammatory proteins such as chemokines, on key vascular biological processes.
These processes include atherosclerosis - the fatty plaque formation responsible for angina and heart attacks, restenosis – the narrowing of the arteries that can occur after stenting, and angiogenesis – the growth of new blood vessels.
A major focus of the group is finding novel ways to hinder inflammatory diseases using chemokine inhibitors. Chemokines are small inflammatory proteins that play a key role in the immune response to injury or infection. They direct the migration of inflammatory cells to sites of vascular injury and play a critical role in the development of inflammatory diseases such as atherosclerosis.
“We are currently looking at unique chemokine inhibitors that can specifically inhibit certain classes of chemokines. We are exploring them as potential therapies to prevent atherosclerosis, cancer and restenosis,” Christina explained.
The team have been investigating the effects of the chemokine inhibitor ‘35K’ on angiogenesis. Early findings suggest that 35K has striking inhibitory effects on the angiogenesis associated with inflammatory conditions, but not in low oxygen conditions where angiogenesis is preserved. This means that 35K inhibits detrimental angiogenesis, which promotes atherosclerosis and cancer, but has no effect on good forms of angiogenesis.
“While new vessel formation after a heart attack will improve long term survival and prognosis, current angiogenesis inhibitors impede angiogenesis across the board, good and bad. Our findings could lead to drugs with significant advantages over current anti-angiogenic therapies,” said Christina.
In an exciting development, the group have a paper under review with the European Heart Journal, controversially suggesting that the protective functions of HDL may be dramatically reduced in advanced atherosclerosis. In epidemiological studies, higher levels of HDL have been strongly associated with a reduced risk of atherosclerosis. Likewise, animal studies have shown consistent benefit of HDL on early atherosclerosis.
“Despite strong epidemiological and experimental evidence of effect, this has not translated into successful therapy for humans with established disease in large scale clinical trials,” explained Christina. “Our studies demonstrate that raising HDL is much more effective at reducing early-stage atherosclerosis than late-stage disease, indicating that the timing of HDL-raising is a critical factor in its protective effects,” Christina said.
The group have also received much acclaim for their work on the role of HDL in wound healing. The group is exploring the topical application of HDL, where the HDL is applied directly to the wound, and its effect on healing capacity. “Wound repair in diabetic patients is severely impaired and can lead to intractable wounds and even amputation,” explained Christina. Impressively, the group have shown that in diabetic patients, HDL can return the impaired angiogenesis to non-diabetic levels, having enormous implications for diabetic wound care.
Another important line of research looks at how HDL might be used to aid recovery and improve outcomes after stent implantation, an operation to place a metal scaffold into a diseased artery to restore blood flow. The group have made the important discovery that HDL bound onto stainless steel, the material used in stents, can prevent blood clotting and smooth muscle cell proliferation, important contributors to restenosis and stent failure. Furthermore, they have identified that infusions of HDL reduce the re-growth of cells following stent implantation.