Saturday, December 18, 2021

Research finds potential mechanism linking autism, intestinal inflammation

Good news! A long and comprehensive article! This research is all based on mouse models.


"Though many people with autism spectrum disorders also experience unusual gastrointestinal inflammation, scientists have not established how those conditions might be linked. Now MIT and Harvard Medical School researchers, working with mouse models, may have found the connection: When a mother experiences an infection during pregnancy and her immune system produces elevated levels of the molecule Interleukin-17a (IL-17a), this can not only alter brain development in her fetus, but also alter her microbiome such that after birth the newborn’s immune system can become primed for future inflammatory attacks. ..."

From the abstract:
"Children with autism spectrum disorders often display dysregulated immune responses and related gastrointestinal symptoms. However, the underlying mechanisms leading to the development of both phenotypes have not been elucidated. Here, we show that mouse offspring exhibiting autism-like phenotypes due to prenatal exposure to maternal inflammation were more susceptible to developing intestinal inflammation following challenges later in life. In contrast to its prenatal role in neurodevelopmental phenotypes, interleukin-17A (IL-17A) generated immune-primed phenotypes in offspring through changes in the maternal gut microbiota that led to postnatal alterations in the chromatin landscape of naive CD4+ T cells. The transfer of stool samples from pregnant mice with enhanced IL-17A responses into germ-free dams produced immune-primed phenotypes in offspring. Our study provides mechanistic insights into why children exposed to heightened inflammation in the womb might have an increased risk of developing inflammatory diseases in addition to neurodevelopmental disorders."

Research finds potential mechanism linking autism, intestinal inflammation | MIT News | Massachusetts Institute of Technology Infection during pregnancy with elevated levels of the cytokine IL-17a may yield microbiome alterations that prime offspring for aberrant immune responses, mouse study suggests.

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