Would you believe a parasitic worm might actually treat crohn’s disease? Previously, worm infections were known to increased susceptibility of multiple parasite infections. Now current research has scientists reevaluating the symbiotic relationship between humans and infectious worms. Dr. P’ng Loke, a parasite immunologist at New York University School of Medicine, conducted an experiment on two different parasitic worms effects on mice digestive systems and the human digestive system. Specifically looking at a mutation of Nod2 gene in mice; a similar mutation in humans is associated with crohn’s disease. Crohn’s disease is an inflammatory bowel disease (IBD) that causes inflammation of the lining of the digestive tract. Patient’s symptoms include: abdominal pain, severe diarrhea, fatigue, weight loss and malnutrition.
During the experiment Nod2 mutant mice showed a defect in the small intestine goblet cells responsible for producing a mucus layer (Figure 1B). The lack of mucus creates the perfect environment for the bacteria Bacteroides vulgatus. This bacteria causes inflammation leading to intestinal damage observed in crohn’s patients. Next the mutant mice were infected with whipworm (Trichuris muris) or a corkscrew-shaped worm (Heligmosomoides polygyrus). Three phenomena were observed post-infection: one, infected mutants had an increase in mucus production as compared to the non-infected mutants (Figure1C). Two, a decrease in the inflammation causing bacteria, B. vulgatus. Three, the mucus-environment is conducive to a mucus eating bacteria called Clostridiales bacteria. This bacterium is associated with inflammation reducing properties. The shift in environment and population is referred to as a type-2 immune response. The parasitic worms causes a host immune response of T- helper cells, which release chemicals called interleukin-4 and interleukin-13. These chemicals are known for the mucus production; B. vulgatus inhibits the production of these immune chemicals. With an increase in mucus, the Clostridiales bacteria are able to outcompete Bacteroidales bacteria. This symbiotic web is a great example of host manipulation. It’s similar to multiple infection strategy, the parasitic worm manipulates the host’s immune system, causing a decrease in Bacteroidales bacteria and a hitchhiker/ “lucky passenger” or Clostridiales bacteria is able to benefit from the manipulating (competition elimination). With an increase of “good” bacteria the wild-type function is restored.
The second experiment was conducted on humans to determine if the same relationship in mice was observed. First scientist acquired fecal samples from people in Malaysia infected with parasitic worms. A second sample was taken after administration of a deworming drug. By analyzing the amount of whipworm eggs present in the specimen, it was determined that people had less Clostridiales and more Bacteriodales bacteria than before drug treatment. This demonstrates ridding the worms would result in a high B. vulgatus environment, inflammation occurs, and intestinal damage develops leading to crohn’s.
These results of course do not imply that if you suffer from crohn’s to go infect yourself with a parasitic worm. For now further research of this symbiotic web, specifically parasitic manipulation will lead to drug treatment for crohn’s and possible other inflammatory dowel diseases.
Original article: Here
More about parasitic worms: Here