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"... Infections during pregnancy can lead to high levels of the inflammatory signaling molecule interleukin-17a (IL-17a), which can not only affect brain development in the fetus, but also alter the maternal microbiome in a way that primes the newborn’s immune system for future inflammatory attacks. ...
“We’ve shown that IL-17a acting on the fetal brain can induce autism-like behavioral phenotypes such as social deficits,” ... “Now we are showing that the same IL-17a in mothers, through changes in the microbiome community, produces comorbid symptoms in the offspring, specifically a primed immune system.”"
“We’ve shown that IL-17a acting on the fetal brain can induce autism-like behavioral phenotypes such as social deficits,” ... “Now we are showing that the same IL-17a in mothers, through changes in the microbiome community, produces comorbid symptoms in the offspring, specifically a primed immune system.”"
From the abstract:
"Children with autism spectrum disorders often display dysregulated immune responses and related gastrointestinal symptoms. ... 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. ... 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."
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