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Wellcome Trust Research Round-up 27.07.15

27 Jul, 2015

Our fortnightly round-up of news from the Wellcome Trust Community

Worldwide genetic link discovered for Inflammatory Bowel Disease

L0012304 T. Willis; stomach from "Pharmaceutice rationalis", 1674The underlying genetics of Inflammatory Bowel Disease (IBD) are consistent around the world, and across diverse populations, according to a new study from the Wellcome Trust Sanger Institute.

The research, published in the journal Nature Genetics, identified 38 new regions of the genome that are associated with increased risk of IBD.

Scientists analysed10,000 DNA samples from people of East Asian, Indian and Iranian descent, as well as an existing set of 84,640 samples from Europe, in the first genetic study of IBD to include individuals from diverse populations.

Researchers had previously identified 163 variants in the genome that conferred a greater risk of IBD, however this large-scale research had only ever been conducted in Europe. The inclusion of the non-European samples, allowed a further 38 regions to be identified, though this is thought to be due to the increased sample size, rather than regional differences.

Despite the similarities, researchers did identify variants in a gene called NOD2 which increases risk of the disease in Europeans but these variants are not present in Asian populations. At other genetic locations, the variants are present in both European and East Asian samples but seem to have a much stronger effect on disease risk in Asian populations.

“The prevalence of IBD has increased dramatically in Asia over the last 50 years, probably due to lifestyle changes brought about by economic growth” says Dr Carl Anderson, a corresponding author from the Wellcome Trust Sanger Institute.

“We are now able to compare genetic risk profiles of IBD across diverse populations to find out how similar they are. Discovering differences can provide us with biological insights that would be missed if we were to focus our efforts on just a single population. In turn, this can lead to the identification of new drug targets.”

Repairing liver damage with stem cells

L0062836 Degeneration of the liverThe livers of mice with severe liver failure have been repaired using stem cells in a major new study published in Nature Cell Biology.

The study is the first of its kind to restore function to a severely damaged liver in live animals using stem cells. It is hoped that if the technique can be shown to be effective in humans, it could offer a potential alternative to liver transplants in future.

Although the liver is able to repair itself, diseases such as cirrhosis or acute liver failure leave it damaged beyond repair. Scientists transplanted liver stem cells into mice with liver failure and observed the effect these cells had over several months. They found that major areas of the liver had in fact regrown, increasing the overall function of the liver.

Previously, essential liver cells called hepatocytes had been used for transplantations, but their lack of ability to grow in laboratory conditions limits their use. Liver stem cells are able to grow well in lab conditions and also have the advantage of being able to change into all types of cells required in the liver.

Professor Stuart Forbes, of the MRC Centre for Regenerative Medicine at the University of Edinburgh, said: “Revealing the therapeutic potential of these liver stem cells brings us a step closer to developing stem cell based treatments for patients with liver disease. It will be some time before we can turn this into reality as we will first need to test our approach using human cells. This is much needed as liver disease is a very common cause of death and disability for patients in the UK and the rest of the world’’

New target in the fight against malaria

Amalaria drug that targets a malaria patient’s own proteins rather than the parasite itself may offer a new hope for treatment of the disease.

The new research from the Wellcome Trust Sanger Institute shows how the drug is able to target a human protein relied upon by the malaria parasite to invade our red blood cells. This is especially important given that the rapidly-evolving malaria parasite, Plasmodium falciparum, has rendered front-line antimalarial drug, artemisinin, largely ineffective.

Scientists investigated the PfRH5 protein of the P. falciparum parasite, which must bind to the protein basigin, on the outer surface of our red blood cells in order to invade and infect them. By introducing an antibody that was targeted to the basigin protein, the malaria parasite was effectively blocked from binding to, and invading, red blood cells.

The antibody was also able to efficiently clear already-established malarial disease in mice, with the levels of infection falling to undetectable levels within 72 hours of treatment.

“This counter-intuitive approach to malaria treatment leaves the parasite powerless,” explains Dr Zenon Zenonos, a first author from the Wellcome Trust Sanger Institute. “If the parasite can’t bind to the surface of our red blood cells and invade, it can’t reach the next stage in its lifecycle, so it dies. There’s nothing the parasite can do to get round it, as the interaction is absolutely essential for infection to occur.”

This research is published in the Journal of Experimental Medicine.

In other news…

Congratulations to Professor Emilie Savage-Smith and Professor Simon Swain who have been elected Fellows of the British Academy for the humanities and social sciences. The researchers, from the University of Oxford and the University of Warwick respectively, hold a joint Wellcome Trust Senior Investigator Award for a project titled “A Literary History of Medicine: The Best Accounts of the Classes of Physicians by Ibn Abi Usaybi`ah (d. 1270)”.

Image credits: (from top to bottom) Wellcome Library, London; St Bartholomew’s Hospital Archives & Museum, Wellcome Images, Wellcome Images; Mosquito that causes malaria by NIAID via Flickr CC-BY

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