Research led by the University of Virginia School of Medicine in the United States has revealed a potentially key link that could shed new light on the complex mechanisms underlying the development of autism. The study, led by researcher John Lukens, PhD, highlights the influence of maternal gut microbiota and the immune system molecule interleukin-17a (IL-17a) as factors that may contribute to the development of autism-like neurological conditions.
The research, carried out on animal models (laboratory rats), suggests that the mother’s microbiota – the set of microorganisms that inhabit her intestine – may have a more decisive impact on the likelihood of developing autism in her offspring than the individual’s own microbiota.
One of the central findings of the study points to interleukin-17a (IL-17a), an inflammatory molecule produced by the immune system, as a possible causative agent. The scientists observed that when IL-17a was suppressed in laboratory mice, their offspring exhibited neurotypical behaviors.
However, in a different scenario, offspring born to mothers with a gut microbiota that predisposed them to an inflammatory response triggered by IL-17a later developed a neurological disorder with characteristics similar to autism.
To reinforce the hypothesis of the influence of the microbiota, the researchers performed fecal transplants. When they transferred the microbiota from mice with this inflammatory predisposition to other mice, they found that the offspring of the second group also developed neurological symptoms comparable to those of autism.
Although the results in animal models do not translate directly to humans, this research opens new avenues for understanding the origins of Autism Spectrum Disorder and may lead to new prevention or intervention strategies focused on gut health and the maternal immune system in the future. The researchers emphasize the need for further studies to validate these findings in humans.
