In the last couple of months, I’ve written several times about maternal immune activation (MIA) and the detrimental effects on the fetus.
Read here, for example, about the relationship of maternal infection to autism. Summarizing that research: infecting pregnant mice with a virus (i.e. stimulating their inflammatory response) led to autistic-like behaviors in the pups. Giving the mothers a gut-antibiotic led to normal pups, the implication being that perhaps some specific species of “bad” bacteria lead to exaggerated immune response in the mothers and babies.
I’ve also described several times how alterations to the maternal microbiome cause microbiome and immune abnormalities in the baby. In fact, earlier this week I wrote about how antibiotics in pregnancy lead to an increased risk of IBD in the children during their lives. Completely coincidentally, yesterday morning I also posted an article on this blog’s Facebook page about how antibiotics given to the mom during labor “delay” a healthy gut microbiome in the baby…the long-term health implications of which are still mostly unknown.[i]
Multiple times, too, I have mentioned how low levels of the regulatory cytokine IL-10, which helps modulate the inflammatory response, is a key player in all this. Low levels of IL-10 in the mother increase the risks (associated with antibiotic use) to their babies.
As helminths are one of the strongest stimulators of the production of regulatory cytokines, the loss of our native macrobiomes in the industrialized world has likely predisposed us toward low IL-10 levels.
With all this new research coming out at once, I just keep thinking about an article published last year…
In light of the fact that hyper-immune responses early in life “…affect the brain, especially neurodevelopment, and increasing evidence links early-life infection [which would cause an inflammatory response] to cognitive and neurodevelopmental disorders,” in 2015, researchers, including my friend, Dr. William Parker at Duke University, did several experiments in rats.[ii] These researchers had previously shown that bacterial infection in newborn rats led to a life-long vulnerability to cognitive dysfunctions. There was a perpetual hypersensitivity of the microglia. (The microglia are the immune cells of the brain.) To sum up: if there was early life infection, these brain immune cells would cause a hyperactive inflammatory response in the brain, affecting brain development.
These scientists then, in this subsequent experiment, showed that inoculating pregnant rats with helminths, “…attenuated the exaggerated brain cytokine response of their offspring to bacterial infection” and more than that: inoculating the babies after weaning, “…completely prevented enduring microglial sensitization and cognitive dysfunction in adulthood.”
Amazing stuff, huh?
[ii] Williamson, LL, McKenney, EA, Holzknecht, ZE, Belliveau, C, Rawls, JF, Poulton, S, Parker, W, Bilbo, S. Got Worms? Perinatal exposure to helminths prevents persistent immune sensitization and cognitive dysfunction by early-life infection. Brain, Behavior, and Immunity. 2016;51:14-28. doi: 10.1016/j.bbi.2015.07.006
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