Infection-Autism Link Explained?

A mouse study suggests a mechanism by which severe infections during pregnancy increase autism risk. 

By | January 31, 2016

FLICKR, ANGELADELLATORREAn immune effector molecule called interleukin 17 (IL-17), produced as part of a mother’s inflammatory reaction to a pathogen, can interfere with her baby’s brain development, according to a mouse study published this week (January 28) in Science. Blocking IL-17 production in pregnant mice prevented the development of autism-like behaviors in their offspring. The results suggest a possible explanation for the fact that women in Denmark who were hospitalized due to an infection during their pregnancy were more likely to have a child with autism.

“In the mice, we could treat the mother with antibodies that block IL-17 after inflammation had set in, and that could ameliorate some of the behavioral symptoms that were observed in the offspring,” coauthor Gloria Choi, an assistant professor at MIT, said in a press release.

Choi’s former Caltech advisor, Paul Patterson, had previously discovered a link between the immune signaling molecule IL-6 and autism-like behavior in rodents. To figure out why, Choi and her colleagues disabled Th17 cells, which are activated by IL-6, in pregnant mice, then triggered an inflammatory response. Lo and behold, the animals’ offspring showed no behavioral abnormalities. The researchers could also eliminate the autism-like behaviors in the mice’s offspring when they treated the mothers with an antibody that blocks IL-17.

“Our data suggest that therapeutic targeting of TH17 cells in susceptible pregnant mothers may reduce the likelihood of bearing children with inflammation-induced ASD [autism spectrum disorder]-like phenotypes,” the authors wrote in their paper.

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