To test their hypothesis that autism may be triggered by the IL-17a molecule, the team blocked IL-17a in lab mice. The researchers recruited female mice from two separate laboratories – those from the first contained microflora in the gut that made them prone to an IL-17a-induced inflammatory response, whereas those from the second (the control) did not.
When the IL-17a molecule was artificially blocked (preventing IL-17a-induced inflammatory responses), the pups from both sets of mice were born with neuro-typical behaviors. Yet, when everything was left to progress without additional human intervention, the pups born from mothers in the first group went on to develop an autism-like neurodevelopmental condition, which affected social and repetitive behaviors.
To confirm that this was due to the group’s unique microflora, the researchers performed a fecal transplant on mice from the second group using the feces of the mice from the first group. The idea here is to change the microflora of the second group so that it more closely resembles that of the first. And, as expected, the pups from the second group went on to develop an autism-like neurodevelopmental condition.