In recent years, scientists have increasingly uncovered links between gut microbiota—the trillions of microorganisms in our digestive system—and overall health. These microbes have been shown to influence everything from mental well-being and stress response to the likelihood of developing autoimmune conditions such as rheumatoid arthritis and type 1 diabetes.
Now, a new study published in The Journal of Immunology sheds light on a possible connection between the microbiome and autism.
Autism, as defined by the World Health Organization (WHO), refers to a diverse group of developmental conditions that affect communication and social interaction. WHO also notes that individuals with autism often experience co-occurring conditions, including epilepsy, anxiety, depression, attention deficit hyperactivity disorder (ADHD), sleep difficulties, and self-injurious behavior. Intellectual ability among individuals on the autism spectrum varies widely.
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The recent study suggests that a child’s likelihood of developing autism may be more influenced by their mother’s gut microbiota than by their own.
“The microbiome can shape the developing brain in multiple ways,” said John Lukens, PhD student and lead researcher from the University of Virginia School of Medicine. “It plays a crucial role in calibrating how an offspring’s immune system responds to infections, injuries, and stress.”
A key molecule at the center of this research is interleukin-17a (IL-17a), a cytokine produced by the immune system. IL-17a has already been linked to conditions such as psoriasis, multiple sclerosis, and rheumatoid arthritis, and plays an essential role in defending the body against fungal infections. Importantly, it may also influence brain development in the womb.
To explore this, researchers studied mice with differing gut microbiota. One group harbored bacteria that triggered a stronger inflammatory response involving IL-17a, while the control group did not. When IL-17a activity was artificially suppressed in the offspring, both groups initially displayed neurotypical behavior. However, once the mice matured naturally without intervention, those from the first group exhibited autism-like traits, such as repetitive behaviors.
In a follow-up experiment, researchers transplanted fecal matter from the first group into the control group, effectively transferring the pro-inflammatory gut bacteria. As a result, the previously unaffected mice also began to display autism-like behaviors.
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Although these findings are based on animal studies, they lay important groundwork for future research into how maternal gut health may influence the risk of neurodevelopmental disorders in humans.
“In terms of translating our work to humans, the next big step is identifying microbiome features in pregnant women that correlate with autism risk,” Lukens said. “The goal is to determine how we can safely and effectively modulate the maternal microbiome.”
While targeting IL-17a might offer one potential path for intervention, Lukens cautioned against manipulating the immune system during pregnancy due to the delicate balance required to maintain embryonic health. “Pregnancy is a unique immune state,” he explained. “The body is essentially tolerating foreign tissue—the baby—so immune regulation is complex and sensitive.”
He added that IL-17a is just one piece of a much larger puzzle. “There are many other molecules that warrant exploration.”
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