To explore their theory that IL-17a might be a trigger for autism, researchers conducted tests using lab mice. They brought in female mice from two different labs: one group had gut microflora that made them more likely to have an inflammatory response triggered by IL-17a, while the control group—sourced from the second lab—did not show that same sensitivity.

When the IL-17a molecule was intentionally blocked—thereby halting the inflammatory responses it triggers—the offspring of both groups of mice were born displaying typical, healthy behaviors. However, when no intervention was made and things were allowed to proceed naturally, the pups born to mothers in the first group went on to show signs of an autism-like neurodevelopmental disorder, marked by changes in social behavior and repetitive actions.

To test whether the unique gut microbiome of the first group was the cause, the researchers conducted a fecal transplant. They transferred fecal matter from the first group to mice in the second group, essentially altering the microbiome of the second group to match the first. As anticipated, the pups in the second group subsequently developed similar autism-like neurodevelopmental symptoms.

These are still early-stage studies and might not directly apply to human pregnancies, but they open up an intriguing path for autism research. They also offer compelling evidence that a mother’s gut health could play at least a partial role in the development of neurodevelopmental conditions.

According to Lukens, the next step is to investigate whether similar patterns can be found in humans and to identify what specific elements in the mother’s microbiome may be linked to autism. He also noted that there are a number of other molecules worth looking into, adding that IL-17a could be just one small part of a much more complex picture.