Summary: A new study from the University of Utah Health reveals a strong influence of gut microbes on behavior. In mice, recurring gastrointestinal (GI) distress reduced social engagement—an effect that persisted after GI symptoms resolved—and introducing specific bacterial strains reversed both intestinal injury and the associated social changes.
This research highlights the gut microbiome as a potential contributor to symptoms linked with autism spectrum disorder (ASD) and suggests microbiome-based interventions could relieve both GI problems and related behavioral alterations.
Key Facts:
- Gut–behavior connection: Repeated colitis in mice produced lasting reductions in social interaction, mirroring social challenges often observed in ASD.
- Microbial intervention: Supplementing mice with selected human-derived bacterial species lessened intestinal damage and improved social engagement after colitis.
- Therapeutic potential: Identifying protective gut microbes points toward personalized microbiome therapies to address gastrointestinal and behavioral symptoms in ASD and related conditions.
Source: University of Utah
Background: Many people with autism experience chronic GI issues such as constipation, diarrhea, and abdominal pain. Clinicians and researchers have debated whether these gastrointestinal symptoms arise from autism’s behavioral or sensory features—or whether GI problems themselves can worsen behavioral traits. The new study provides experimental evidence that gut inflammation can influence social behavior and that certain gut microbes can protect against these effects.
Researchers led by microbiologist June Round, Ph.D., studied how repeated intestinal inflammation affects social interactions in mice and whether microbes from people with or without ASD influence those outcomes. Their results, published in Nature Communications, show that modifying the gut microbiome can alter both gut health and social behavior in a controlled laboratory setting.
The gut–behavior connection
To disentangle the relationship between GI distress and social behavior, graduate student Garrett Brown, Ph.D., induced colitis in mice, which produced pain, diarrhea, and intestinal damage. After repeated inflammatory episodes and a recovery period, the mice showed normal movement and no increased anxiety-like behavior, but they spent less time interacting with unfamiliar mice than controls.
This selective reduction in sociability suggested that the experience of gut inflammation—rather than general malaise—specifically affected social motivation. Because prior work has documented differences in gut microbial communities between autistic and neurotypical individuals, the team investigated whether those microbial differences might influence susceptibility to colitis and its behavioral consequences.
Brown transplanted stool samples from people with autism and from their neurotypical family members into germ-free mice. When colitis was induced, mice colonized with microbiota from autistic donors experienced more severe intestinal damage and greater weight loss than mice colonized with microbiota from neurotypical relatives, indicating a protective role for certain microbial communities.
Identifying protective microbes
Human gut communities are highly complex, so the researchers compared microbial profiles from autistic individuals, their neurotypical family members, and the mice colonized with those communities. Their goal was to identify individual microbes that were more abundant in neurotypical samples and that might confer protection against inflammation.
The analysis highlighted two groups of bacteria. Species of the genus Blautia were consistently more common in neurotypical family members than in their autistic relatives. Separately, higher levels of Bacteroides uniformis in some transplanted mice correlated with less severe colitis. B. uniformis has been implicated in intestinal health in other human GI disorders, suggesting a broader protective role.
When researchers administered isolates of Blautia and Bacteroides uniformis to mice before inducing colitis, both treatments reduced the severity of intestinal injury. Importantly, Blautia supplementation also improved social engagement: mice that received Blautia were more likely to interact with unfamiliar mice after experiencing colitis.
Toward personalized microbiome therapies
This study is among the first to show that specific human-derived gut bacteria can counteract a behavioral deficit tied to prior intestinal distress. As June Round emphasizes, the work points to situations where missing beneficial microbes contribute to disease and where restoring those microbes may be therapeutic.
Further research is needed to determine whether increasing Blautia or Bacteroides uniformis in people could benefit those with GI disorders, autism, or related conditions. Nonetheless, isolating individual protective strains is a crucial step toward personalized, microbiome-targeted treatments. The ultimate goal is rapid microbiome profiling that identifies missing beneficial organisms and replaces them safely and effectively.
About this microbiome, ASD, and behavioral research news
Author: Jennifer Michalowski
Source: University of Utah
Contact: Jennifer Michalowski – University of Utah
Image: The image is credited to Neuroscience News
Original Research: Open access. “Colitis reduces active social engagement in mice and is ameliorated by supplementation with human microbiota members” by June Round et al., Nature Communications.
Abstract
Colitis reduces active social engagement in mice and is ameliorated by supplementation with human microbiota members
Multiple neurological disorders are associated with gastrointestinal (GI) symptoms, including autism spectrum disorder (ASD), but it remains unclear whether GI distress itself can change behavior. The study shows that mice experiencing repeated colitis display reduced active social engagement—measured by interactions with an unfamiliar mouse—even after colitis signs have resolved.
Transplantation experiments into germ-free male mice revealed that microbiota from individuals with ASD worsened gut injury relative to microbiota from familial neurotypical controls. The researchers found enrichment of Blautia species in neurotypical controls and an association between higher Bacteroides uniformis abundance and reduced intestinal injury. Oral administration of either microbe reduced colon injury, and a Blautia isolate specifically rescued the colitis-associated social deficit. Overall, the data demonstrate that past intestinal distress can alter social behavior in mice and that supplementation with specific human microbiota members can ameliorate both gut injury and associated behavioral changes.