From genes to latrines—Vikings and their worms provide clues to emphysema

February 4, 2016

In a paper published today in Scientific Reports a group of researchers led by LSTM have found that the key to an inherited deficiency, predisposing people to emphysema and other lung conditions, could lie in their Viking roots.

Archaeological excavations of Viking latrine pits in Denmark have revealed that these populations suffered massive worm infestations http://sciencenordic.com/dna-study-vikings-were-plagued-intestinal-parasites. The way that their genes developed to protect their from disease caused by worms has become the inherited trait which can now lead to in .

Chronic (COPD) and emphysema affect over 300 million people, or nearly 5% of the global population. The only inherited risk factor is alpha-1-antitrypsin (A1AT) deficiency, and this risk is compounded if individuals smoke tobacco.

A1AT protects the lungs and liver from enzymes called proteases that are produced by cells of the immune system, but also by parasitic worms. In the absence of A1AT these proteases can break down lung tissue leading to COPD and emphysema.

Deficiency of A1AT is genetically determined and is due to deviants of A1AT that are surprisingly common, particularly in Scandinavia, where they evolved in Viking populations more than two thousand years ago. Why these disease-causing deviants of A1AT are so common in human populations today has long been a mystery.

LSTM's Professor Richard Pleass is senior author on the paper. He said: "Vikings would have eaten contaminated food and parasites would have migrated to various organs, including lungs and liver, where the proteases they released would cause disease."

In this latest paper the authors show that these deviant forms of A1AT bind an antibody called immunoglobulin E (IgE) that evolved to protect people from worms. The binding of A1AT to IgE prevents the antibody molecule from being broken down by such proteases.

"Thus these deviant forms of A1AT would have protected Viking populations, who neither smoked tobacco nor lived long lives, from worms." Continued Professor Pleass, "it is only in the last century that modern medicine has allowed human populations to be treated for disease causing worms. Consequently these deviant forms of A1AT, that once protected people from parasites, are now at liberty to cause and COPD."

Explore further: New collaboration to develop treatments for liver disease

More information: Phyllis M. Quinn et al. IgE-tailpiece associates with α-1-antitrypsin (A1AT) to protect IgE from proteolysis without compromising its ability to interact with FcεRI, Scientific Reports (2016). DOI: 10.1038/srep20509

Related Stories

A speedy test for bladder cancer

January 14, 2015

A fast and accurate urine test for bladder cancer developed by A*STAR researchers has the potential to replace the currently used invasive physical probe.

Understanding lung disease in aboriginal Australians

March 2, 2015

A new study has confirmed that Aboriginal Australians have low forced vital capacity—or the amount of air that can be forcibly exhaled from the lungs after taking the deepest breath possible. The finding may account for ...

Recommended for you

New paper answers causation conundrum

November 17, 2017

In a new paper published in a special issue of the Philosophical Transactions of the Royal Society A, SFI Professor Jessica Flack offers a practical answer to one of the most significant, and most confused questions in evolutionary ...

Chance discovery of forgotten 1960s 'preprint' experiment

November 16, 2017

For years, scientists have complained that it can take months or even years for a scientific discovery to be published, because of the slowness of peer review. To cut through this problem, researchers in physics and mathematics ...

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.