The importance of our gut microbiota to our health has become increasingly clear recently as more and more studies have been released. Everything from how we react to fear and negative stimuli to our weight and mental health to our susceptibility to autoimmune disorders like type 1 diabetes and lupus can be impacted.
Using research on animals, a recent study that was published in The Journal of Immunology has discovered a connection between the gut microbiota and the neurodevelopmental disorder autism. However, the researchers claim that our mother’s microbiota has a greater influence on our likelihood of developing autism than does our own.
“The microbiome can shape the developing brain in multiple ways,” John Lukens, lead researcher and PhD student from the University of Virginia School of Medicine, said in a statement.
“The microbiome is really important to the calibration of how the offspring’s immune system is going to respond to an infection or injury or stress.” Regarding autism, this connection might be related to a specific molecule that the immune system produces called interleukin-17a (also known as IL-17a).
The molecule has already been linked to diseases like psoriasis, multiple sclerosis, and rheumatoid arthritis. It has also been demonstrated to play a significant role in preventing infections, particularly fungal infections. Crucially, it can also affect how the brain grows while still within the womb.
The team suppressed IL-17a in lab mice to test their theory that the cytokine may cause autism. Female mice from two different labs were chosen by the researchers; the mice from the first lab had gut microbiota that predisposed them to an inflammatory response triggered by IL-17a, whereas the mice from the second lab (the control) did not.
The pups from both sets of mice exhibited neuro-typical behaviors at birth when the IL-17a molecule was artificially suppressed, hence preventive of IL-17a-induced inflammatory responses. Nevertheless, the pups born to moms in the first group later developed a neurological disorder that resembled autism, affecting social and repetitive behaviors, when everything was allowed to grow without further human interference.
The researchers used the feces of the mice in the first group to perform a fecal transplant on the mice in the second group to verify that this was caused by the group’s distinct microbiota. Here, the goal is to alter the second group’s microflora to more closely match the first. As anticipated, the second group’s pups later developed a neurological disorder resembling autism.
Although these are early studies and might not apply to human pregnancies, they do present an intriguing line of inquiry for autism research and offer compelling evidence that the mother’s gut health contributes to the development of neurodevelopmental disorders to some extent.
The next step, according to Lukens, is to determine what aspect of the mother’s microbiome is linked to the development of autism and see whether they can find such correlations in people. There are a number of more molecules to look at. IL-17a might be a single component in a much bigger picture, Lukens suggested.
