Parasitic Worms May Prevent Crohn's Disease by Altering Bacterial Balance

The thought of parasitic worms swimming around in some people's intestines may be revolting, but they seem to forestall Crohn's disease and other various types of inflammatory bowel disease (IBD). A new study may explain how this works, which will reveal how worms enable microbes in the intestines to fight bacteria that promote inflammation.

In people with IBD, inflammation in the digestive tract usually results in bleeding and diarrhea which can sometimes lead to intestinal obstructions or other severe complications. Because parasitic worms can be harmful, they are unlikely allies against these diseases. IBD is rare in parts of the world where parasitic worms are prevalent. But, in more developed parts of the world where less people carry these parasites in their intestines, IBD is much more common.

To determine the "frenemy" relationship between our intestines and these parasites, immunologist Ken Cadwell and colleagues tested mice with the same genetic defect found in many humans with Crohn's disease. Mucus-secreting cells in the intestines malfunction in these animals, which reduces the amount of mucus secreted to protect the lining of the gut from harmful bacteria. Researchers also found a change in the rodents' microbiome. The abundance of a microbe, an inflammation-inducing bacterium found in the Bacteroides, soars in the mice with genetic effect. 

The researchers found that feeding the rodents one type of intestinal worm restored their mucus-producing cells to normal. At the same time, the levels of two different indicators declined in the animals' intestines. In addition, the bacterial lineup in the rodents' guts shifted. Bacteroids's numbers plunged, yet the prevalence of the Clostridiales, a species in a different microbial group, increased. A second species of worm also triggers similar changes in the mice's intestines. 

To check if these parasites cause the same effect in humans, the scientists compared two populations in Malaysia. One group consisted of urbanites living in Kuala Lumpur, who have few intestinal parasites. The second group consisted of an indigenous group, the Orang Asli, who live in a rural area where the parasites are widespread. A type of Bacteroides, the pro inflammatory microbes, predominated in the people of Kuala Lumpur. It was more rare among the Orang Asli, where Clostridiales was common. Treating the Orang Asli with drugs to kill their intestinal worms reversed this pattern, favoring Bacteroides species over Clostridiales species. The team analyzed two sets of data on the frequencies of different intestinal microbes, which included U.S. residents who were healthy, and children in North America who have IBD. They saw the same inverse relationship, where Clostridiales species are up and Bacteroides are down, and vice versa. 

The study's findings suggest that parasitic worms deliver their benefits through their impact on the microbial mixture in the intestines. But, the researchers caution that direct evidence is still warranted to show that Bacteroides species are responsible for Crohn's disease. Also, turning the results into clinical treatment may be difficult, because recent clinical trials were disappointing. The researchers indicated that worm therapy might only work on roughly 30% of people suffering from Crohn's disease, who have the same genetic flaw as the mice tested. 

I think this data is very interesting, and the correlation seems promising, but this treatment may not be realistic for many with Crohn's disease because people may not agree to this treatment. On paper this sounds like a great, natural treatment, but there also may be complications of these parasites inside the body that have not been researched or tested. I cannot imagine that the majority of Crohn's patients would choose to have these worms inside of them, over taking other medications to control their symptoms. Again, I believe these various studies are promising and do show correlation, but more research is definitely warranted, and may not be clinically realistic.