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.
