Study identifies possible connection to autism development

In recent years, several studies have highlighted the link between our gut microbiota and our general health.

From our mental health to our responses to stress and our susceptibility to autoimmune disorders like rheumatoid arthritis and type 1 diabetes, the influence of our gut flora is extensive.

A new study featured in The Journal of Immunology provides new perspectives on the connection between the microbiome and autism.

The World Health Organization describes autism as a varied set of conditions associated with brain development that impact social interaction and communication.

Additionally, the WHO indicates that individuals with autism “frequently experience co-occurring conditions, such as epilepsy, depression, anxiety, and attention deficit hyperactivity disorder, along with challenging behaviors like trouble sleeping and self-harm.” The intellectual abilities of these individuals vary from one person to another.

Research indicates that the microbiota of our mothers may have a more significant impact on the development of autism than our own microbiota.

John Lukens, the lead researcher and PhD student at the University of Virginia School of Medicine, stated, “The microbiome can influence the developing brain in various ways.”

He further explained, “The microbiome plays a crucial role in determining how the immune system of the offspring will react to infections, injuries, or stress.”

A potential link between the microbiome and autism could be a molecule produced by the immune system known as interleukin-17a, or IL-17a.

Up to now, studies have indicated that this cytokine is involved in conditions like psoriasis, multiple sclerosis, and rheumatoid arthritis, and it plays a crucial role in protecting the body from fungal infections. Additionally, it seems to affect brain development during pregnancy.

Researchers conducted their studies on mice with varying gut microbiota. One group had bacteria associated with a heightened inflammatory response triggered by IL-17a, while the control group did not have this.

When IL-17a was artificially suppressed in the pups, both groups exhibited neurotypical behavior. However, once the human intervention ceased and the mice were allowed to develop naturally, those from the first group began to show autism-like symptoms, including repetitive behaviors.

Subsequently, scientists utilized the feces from the first group of mice to carry out a fecal transplant on the second group, successfully transferring the pro-inflammatory gut bacteria. As anticipated, the mice in the second group also began to exhibit behaviors similar to autism.

Although the study has only been performed on mice, it lays the groundwork for additional research that could reveal how much the mother’s gut health influences the onset of neurodevelopmental disorders.
“In terms of applying our findings to humans, I believe the next significant step would be to pinpoint characteristics of the microbiome in expectant mothers that are linked to autism risk,” Lukens stated. “The crucial aspect is to determine what methods can be used to effectively and safely adjust the microbiome in the mother.”

While inhibiting IL-17a may also provide a means to avert autism, Lukens noted that it carries certain risks. “Considering pregnancy, the body is essentially accepting foreign tissue, which is the baby,” he explained. “Consequently, maintaining the health of the embryo requires a delicate balance of immune regulation, so individuals often hesitate to alter the immune system during pregnancy.”

He mentioned that there are many other molecules worth investigating, as IL-17a represents only a small fragment of a much larger picture.

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