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Colitis reduces active social engagement in mice and is ameliorated by supplementation with human microbiota members
D Garrett Brown1, Michaela Murphy1, Roberto Cadeddu2
1Department of Pathology, University of Utah School of Medicine, Huntsman Cancer Institute, Division of Microbiology and Immunology, Salt Lake City, UT, USA.
Abstract:
Multiple neurological disorders are associated with gastrointestinal (GI) symptoms, including autism spectrum disorder (ASD). However, it is unclear whether GI distress itself can modify aspects of behavior. Here, we show that mice that experience repeated colitis have impaired active social engagement, as measured by interactions with a foreign mouse, even though signs of colitis were no longer present. We then tested the hypothesis that individuals with ASD harbor a microbiota that might differentially influence GI health by performing microbiota transplantation studies into male germfree animals, followed by induction of colitis. Animals that harbor a microbiota from ASD individuals have worsened gut phenotypes when compared to animals colonized with microbiotas from familial neurotypical (NT) controls. We identify the enrichment of Blautia species in all familial NT controls and observe an association between elevated abundance of Bacteroides uniformis and reductions in intestinal injury. Oral treatment with either of these microbes reduces colon injury in mice. Finally, provision of a Blautia isolate from a NT control ameliorates gut injury-associated active social engagement in mice. Collectively, our data demonstrate that past intestinal distress is associated with changes in active social behavior in mice that can be ameliorated by supplementation of members of the human microbiota.
Insights
Past gastrointestinal distress in mice impairs social behavior. Supplementing with specific human gut microbes, like Blautia, can restore social engagement and reduce gut injury, suggesting a microbiota link to neurological conditions.
Area of Science:
- Neuroscience
- Gastroenterology
- Microbiology
Background:
- Neurological disorders, such as autism spectrum disorder (ASD), often present with gastrointestinal (GI) symptoms.
- The impact of GI distress on behavior, particularly social engagement, remains incompletely understood.
- Investigating the gut microbiome's role in modulating GI health and its connection to neurological conditions is crucial.
Purpose of the Study:
- To investigate if prior gastrointestinal distress influences social behavior in mice.
- To determine if the human gut microbiota, particularly from individuals with ASD, affects GI health and behavior.
- To identify specific microbial species that can mitigate GI injury and associated behavioral changes.
Main Methods:
- Induction of repeated colitis in mice to assess long-term effects on social behavior.
- Microbiota transplantation studies using germ-free animals colonized with microbiota from ASD and neurotypical (NT) individuals.
- Induction of colitis post-transplantation to evaluate gut phenotypes and behavioral outcomes.
- Identification and oral administration of specific bacterial species (Blautia, Bacteroides uniformis) to assess their therapeutic potential.
Main Results:
- Mice with a history of colitis exhibited impaired active social engagement, even after colitis resolution.
- Animals colonized with microbiota from ASD individuals showed worsened gut phenotypes compared to those with NT microbiota.
- Enrichment of Blautia species was observed in NT controls, and Bacteroides uniformis abundance correlated with reduced intestinal injury.
- Oral administration of Blautia or B. uniformis reduced colon injury in mice.
- Supplementation with a Blautia isolate ameliorated social behavior deficits linked to gut injury.
Conclusions:
- Past intestinal distress can lead to persistent changes in active social behavior in mice.
- The human gut microbiota composition influences GI health and may play a role in ASD-related gut issues.
- Specific gut microbes, such as Blautia and Bacteroides uniformis, demonstrate potential for therapeutic intervention in GI disorders and associated behavioral symptoms.
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