Helminths and the Microbiome

As promised:  more about how the presence of helminths (a macrobiome) in the gut improves the quality of the microbiome.

In 2015, Dr. William Parker of Duke University’s Medical School, published a paper in Gut Microbes called, “Alteration of the rat cecal microbiome during colonization with the helminth Hymenolepis diminuta.”[i]  Dr. Parker and colleagues examined the changes to the bacterial content of the rat intestine when colonized with HDs, a mutualistic (beneficial) helminth native to rodents.  They discovered that there was a profound shift in the species of bacteria:

“Colonization of the rats used in this study with Hymenolepis diminuta cause a substantial shift in the microbial community, primarily characterized by changes in the relative contributions from species within the Firmicutes phylum.  Specifically, colonization with the helminth is associated with increased Clostridia and decreased Bacilli.  The contribution of Bacilli to the microbiome is higher with a Western diet characterized by processed sugars and high fat content whereas some species of Clostridia are known to tighten the epithelial barrier and decrease propensity for allergy.”

 An in vivo Australian study[ii] on those with celiac also occurred in 2015.  Volunteers were given Necator americanus (human hookworm).  The researchers assessed the changes in the microbiota before and after colonization, following a gluten challenge: “Experimental hookworm infection of the trial subjects resulted in maintenance of the composition of the intestinal flora, even after a moderate gluten challenge.  Notably, we observed a significant increase in microbial species richness over the course of the trial…”  That is, the presence of a helminth actually improved the diversity of the microbiome, even after the subjects were exposed to an “inflammatory” substance.

In 2016, Dr. P’ng Loke and colleagues at New York University made a similar discovery.  In this study[iii] the researchers looked at mice colonized with Trichuris suis, a porcine whipworm (thus, a non-native helminth).  They found a thousand-fold decrease in Bacteroids, a group of bacterial species linked to inflammatory bowel disease.  They too found an increase (10-fold)  in the number of Clostridia, a species known to counter inflammation. More than that: these researchers found that “Additionally, we show that individuals from helminth-endemic regions harbor a similar protective microbiota and that deworming treatment reduced levels of Clostridiales and increased Bacteroidales.”

Deworming humans – which has no direct effect on the bacterial content of the gut – nonetheless causes an increase in inflammatory and a decrease in anti-inflammatory bacteria. 

Those of us living in the industrialized world have been “dewormed” simply through lack of exposure.  Other than pin worms (which are very undesirable due to the side effects), we have no way of obtaining a macrobiome other than by supplementing. Call me crazy (everyone else does!), but to me, it seems that to not add helminths back into our biomes is the height of illogic.

__________________

[i] Erin A McKenney, Lauren Williamson, Anne D Yoder, John F Rawls, Staci D Bilbo & William Parker (2015). Alteration of the rat cecal microbiome during colonization with the helminth Hymenolepis diminuta, Gut Microbes, 6:3,182-193, DOI: 10.1080/19490976.2015.1047128

[ii] Paul Giacomin, Martha Zakrzewski, John Croese, Xiaopei Su, Javier Sotillo, Leisa McCann, Severine Navarro, Makedonka Mitreva, Lutz Krause, Alex Loukas, Cinzia Cantacessi (2015). Experimental hookworm infection and escalating gluten challenges are associated with increased microbial richness in celiac subjects. Scientific Reports 5, Article number: 13797. doi:10.1038/srep13797

[iii] Deepshika Ramanan, Rowann Bowcutt, Soo Ching Lee, Mei San Tang, Zachary D. Kurtz, Yi Ding, Kenya Honda, William C. Gause, Martin J. Blaser, Richard A. Bonneau, Yvonne AL Lim, P’ng Loke, Ken Cadwell. Helminth infection promotes colonization resistance via type 2 immunity. Science, 2016 DOI: 10.1126/science.aaf3229


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