In a study published recently in the journal Science, researchers from MIT, NYU, and the University of Colorado demonstrated potential causative evidence that severe inflammation in a pregnant mother can lead to an autism spectrum disorder (ASD) in the offspring.
Previous reports have shown a correlation between autism and inflammation. In 2010, a study from Denmark tied infant diagnoses of ASD to a mother’s history of hospitalization due to severe inflammation during pregnancy. More recently, a review paper from Drexel University and the Karolinska Institutet discussed both animal and human evidence showing increased inflammation in the mother due to infection, particularly viral in nature, results in a higher likelihood of the offspring having ASD.
The current study lays out the possible causation behind the development of inflammation-induced ASD. The team had noticed previous reports that rodents challenged with viral-like infection while pregnant were more likely to develop pups with ASD-like behavior. It was later discovered interleukin 6 (IL-6) was a major cause of the increased inflammation, and broadly decreasing the inflammatory response to infection led to a decrease in affected pups.
Looking downstream, the current researchers noticed that IL-6 does not actually increase inflammation itself, but activates T-helper 17 (Th17) cells. These cells, once they encounter an infection, release IL-17, a pro-inflammatory cytokine that recruits white blood cells and other cytokines to help fight the pathogen. The researchers used the same approach as above to induce inflammation (challenging pregnant rodents with virus-like entities), but they also gave the rodents targeted therapies to reduce Th17 cells and/or IL-17. In both cases, the rodents showed significantly reduced inflammation and birthed no pups with ASD-like behaviors.
When they studied the brains of affected rodent pups, the researchers noticed anomalies in the cortex region, which is known to be involved in cognition and sensory processing. This is the same region that is known to be anomalous in human patients diagnosed with ASD. These irregularities in the rodent pup cortex were not observed when the mother was given anti-Th17 or anti-IL-17 therapies.
The study makes clear though that these results should not be viewed as a potential cure for ASD. “[W]e don’t know yet how much of that could be translated into humans,” says Gloria Choi, an assistant professor of brain and cognitive sciences, a member of MIT’s McGovern Institute for Brain Research, and the lead author of the study. But this may result in a possible therapy for some mothers with severe inflammation to reduce the likelihood of having a child with ASD.
Edward Marks is a PhD student at the University of Delaware. His research involves the healing of myocardial tissue after major cardiac events using nanomedicine techniques, with the goal of pushing any advancement directly into the clinic. Edward received his BS from Rutgers University and Masters from the University of Delaware.
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