I have some fascinating new research to report to you on helminths, about which I haven’t written in quite awhile. Last week, in my post about gut bacteria and bile acids, I talked, yet again, about the incredible complexity of the gut ecosystem: today’s work only adds to that confusing mix. Researchers in the Czech Republic wanted to learn more about how helminths and the bacterial microbiome work together to successfully modulate inflammation: “…the aim of this study was to determine whether disruption of the microflora during worm colonization can affect the course of intestinal inflammation.”[i] In order to study this question, antibiotics and/or colitis was induced in rodents, some of whom had helminths some of whom didn’t, for comparative purposes.
Three KEY concepts before I describe their results.
Thus, it makes perfect sense that if the bacterial microbiome is disturbed – one of the 3 legs of that tripartite relationship – the other two will also be affected. Since we already know that helminths exert a powerful anti-inflammatory effect, the question becomes: how much of their effect is reliant upon a healthy microbiome? We know too, as per the above, that the loss of helminths leads to bacterial dysbiosis, so it makes sense that there is a symbiotic relationship between the micro and macrobiomes. Prior research (such as I wrote about here) has shown that helminths improve the quality of the bacterial microbiome. This paper points to a study done on macaques (a primate) with inflammatory bowel disease, which showed “…a shift in bacterial composition during Trichuris trichiura colonization toward the conditions observed in healthy animals.”
Ok, a quick summary then of what they found. They broke the rat up into 4 groups: the first were colonized with HDs and were given antibiotics; the second group was colonized with HDs, and given antibiotics and had colitis induced; the third were colonized and only had colitis induced (no antibiotics); and the last were given only antibiotics and colitis – no HDs. They were attempting to answer two questions: 1. Does disruption of the intestinal microbiota during colonization with HDs affect the course of intestinal inflammation and 2. What changes occur in the intestinal bacterial community from various factors including HD colonization, antibiotics and colitis.
Their results revealed a strange anomaly: in contrast to their previous results, there was no protective effect of H. diminuta on intestinal inflammation in either of the groups affected by colitis (one with antibiotics and one without). Why???? Believe it or not, stress is the believed culprit. “…the prolongation of inflammation is a consequence of stress invoked by additional handling of the rats during antibiotics…or placebo administration. It has been shown that acute and also chronic stress correlates with elevated TNF-alpha levels in rats.” How many times on this blog have I talked about the stress being the silent killer? We all have such a tendency to dismiss “psychological” stressors effects on health but here is yet another concrete example of just how detrimental it really is.
In the groups without the combination of helminths AND antibiotics (that is the group that got helminths and colitis, and the group that got antibiotics and colitis), colitis symptoms were so severe they bordered on necrosis (death of tissue). Interesting, right? That group that both had only mild to moderate inflammation…and the group that did not have colitis induced at all, but got helminths and antibiotics only, there was almost no inflammation present. The presence, or lack thereof, of inflammation seemed to be a major factor in determining the richness of the bacterial microbiome. And, as you’d expect, antibiotics was the single biggest factor.
Thus, they could draw the conclusion that their results “…suggest the possibility of inducing the protective effect of the adult tapeworm by drastically transforming the gut microbiota, which we performed using broad-spectrum antibiotics, during H. diminuta colonization.” However, they go on to say, that a better, more beneficial, approach would be the “…enrichment of the microbiome either with probiotic bacteria or fecal microbiota transplantation, which could also have a beneficial impact on the metabolic homeostasis of the host.” In fact, recent studies “…emphasize the importance of the reliance of helminths on bacterial symbionts…”
The take home message then: the ability of helminths to modulate inflammation is reliant upon its gut co-inhabitants, the bacterial microbiome. This should come as a surprise to exactly no one, when you think about it. (It also really gets me to thinking about all those studies done on only 1 component of the biome. How useful is it really, for example, to test a single strain of one probiotic in isolation then? You do have to wonder.) They evolved together, they work together, and they are inexorably linked. So when you take your helminths, take your probiotics – and when you take your probiotics, take your helminths. Your body will thank you for it!
[i] Jirků M, Lhotská Z, Frgelecová L, Kadlecová O, Petrželková KJ, Morien E, Jirků-Pomajbíková K. Helminth Interactions with Bacteria in the Host Gut Are Essential for Its Immunomodulatory Effect. Microorganisms. 2021 Jan 22;9(2):226. doi: 10.3390/microorganisms9020226. PMID: 33499240.