Parasitic worms remodel human gut microbiome – for the better


It appears the humble roundworm can calm an irritable bowel and influence its microbial population. Belinda Smith reports.


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Trichuris whipworms dwell in intestines, but their beneficial effects seem to reach outside the gut.
THIERRY BERROD, MONA LISA PRODUCTION / SCIENCE PHOTO LIBRARY / GETTY IMAGES

In a parasitic paradox, intestinal worms might actually be good for you. A new study shows roundworm infection promotes the growth of healthy bacteria while dampening a particularly nasty strain, all the while reducing inflammation.

Scientists in Asia and the US, led by New York University's Deepshika Ramanan, found roundworm infection in mice and humans tipped gut microbe balance from bad to beneficial. Published in Science, the research adds to a body of work examining how parasites may one day treat disorders such as allergies and multiple sclerosis.

Autoimmune disorders, where a person's immune system overreacts or starts attacking the body, have surged in Western countries. Crohn's disease inflicts diarrhoea, weight loss, lethargy and rashes upon more than half a million adults in the US.

Such inflammatory bowel disorders are thought to be caused by the gut immune system overzealously attacking the intestinal mucous lining, causing inflammation.

One seemingly unorthodox method for calming the immune response has been intestinal parasites – it is, after all, in their best interests to fly under their host's radar. But what about their effect on the host's microbiome? Given millennia of co-evolution within humans and other animals, can worms exert influence on their microbial housemates?

Ramanan and her colleagues examined mice genetically engineered to have Crohn's disease and measured gut microbe populations in the presence and absence of worms.

Prior to infection with the mouse roundworm Trichuris muris, the mice, thanks to their genetic defect, harboured high levels of a bad bacterium called Bacteroides vulgatus and low levels of the beneficial Clostridiales in their gut.

After infection, though, the microbial scales tipped: B. vulgatus numbers dropped while Clostridiales boomed.

A closer look showed how the parasitic worms stifled B. vulgatus growth. The researchers found more interleukin-4 and interleukin-13 in the wormy mice. These molecules stimulate the growth of helper T cells, a type of immune cell that suppresses the overactive immune response and reduces inflammation.

Ramanan and colleagues then turned to humans and to see what happened to an indigenous population in Malaysia with a high rate of worm infection if their parasites were removed.

When they analysed stool samples before and after worming, they found similar results to the mice. With worms, their gut retained more good bacteria than bad. But after worming, bad bacteria took over.

It's important to note that in the human branch of the study, no information was collected on the prevalence of Crohn's disease in the population, and the researchers didn't examine the subjects' helper T cells either.

Yet it all sounds very promising. So if you have irritable bowel syndrome, should you seek worm infection?

Maybe not just yet. Clinical trials haven't been particularly successful, with only a few people responding positively to worm infection. But those with the same genetic defect as the mice, write the researchers, may have the most to gain from this research.

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Belinda Smith is a science and technology journalist in Melbourne, Australia.
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