To test their theory, the research team blocked IL-17a in pregnant mice. They studied two groups of female mice: one group had a type of gut bacteria that triggered an IL-17a inflammatory response, and the other group (the control) did not.

When IL-17a was blocked in both groups, the offspring showed normal, neurotypical behaviors. But when the process was left to occur naturally, pups born to the first group of mothers (with the inflammatory gut bacteria) developed autism-like traits, especially in their social and repetitive behaviors.

To further test their findings, researchers transferred fecal matter from the first group of mice to the second group, essentially altering the second group’s gut microbiome to resemble the first. The result? Their pups also developed autism-like behaviors—strong evidence pointing to the mother’s gut microbiota as a key influence.

Although these are still early findings based on animal studies, the implications are significant. The study opens up a new direction in autism research, suggesting that the state of the mother’s gut health during pregnancy might play a part in neurodevelopmental outcomes.

Next, Lukens and his team plan to investigate whether similar patterns can be observed in humans and identify what specific elements in the maternal microbiome might be involved. He also notes that IL-17a is likely just one piece of a much larger and more complex puzzle.