A new report, led by Dr. Ken Cadwell from the New York University School of Medicine in New York (USA), has found that a symbiotic relationship between intestinal helminths and host may play a role in inhibiting intestinal inflammatory responses.
Changes in the gut microbiota and decreased exposure to intestinal helminths have been suggested as factors in the increased incidence of inflammatory bowel disease (IBD) in developed nations. In this study, the researchers found that helminths may reduce intestinal inflammatory responses by promoting expansion of bacterial taxa that can induce protective anti-inflammatory responses.
Previously, Ramanan and colleagues found that mice deficient in the gene Nod2 develop abnormalities similar to those seen in Crohn’s disease (CD): small intestinal changes consisting of a compromised layer of mucus and alterations in intestinal goblet cell morphology. These changes allow expansion of the pro-inflammatory commensal Bacteroides vulgatus. On the other hand, chronic infection of these mice with the helminth Trichuris muris restored small intestinal alterations. These results were also confirmed with a second helminth, Heligmosomoides polygyrus. Both parasites induced an increase of type-2 immune response in the lamina propria that inhibited B. vulgatus colonization. During helminth infection, colonization of bacteria from Clostridiales family moved B. vulgatus from its niches. Therefore, both helminth infection and type-2 cytokines inhibit B. vulgatus colonization by allowing expansion of Clostridiales strains. These results suggest that intestinal helminths can manipulate the gut microbiota in a way that is beneficial for its host.
IBD is less prevalent in regions where helminth infection is endemic. The researchers analysed stool samples collected from helminth-colonized individuals in Malaysia before and after deworming treatment. They observed that deworming treatment reduced two members of the order Clostridiales (Dialister and Coprococcus) and increased Bacteroidales species (Prevotella). These data support the hypothesis that helminth infection promotes the expansion of Clostridiales communities that compete with pro-inflammatory Bacteroidales species.
To sum up, intestinal helminth infection may inhibit pro-inflammatory bacterial taxa colonization through a type-2 immune response, although this has not been confirmed causally when it comes to humans. Therefore, exposure to intestinal helminths emerges as a protective factor in reducing inflammatory responses and the pathogenesis of inflammatory bowel disease.
Ramanan D, Bowcutt R, Lee SC, et al. Helminth infection promotes colonization resistance via type 2 immunity. Science. 2016; 352(6285):608-12. doi:10.1126/science.aaf3229.
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