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THE ROLE OF GUT IMMUNITY IN THE DEVELOPMENT OF SCHIZOPHRENIA
Soraia de Jesus Fariaand 4 co-authors
University of Coimbra, Center for Neurosciences and Cell Biology (CNC), Laboratory of Immunology and Oncology
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS01-07AM-494
Presentation
Date TBA
Board: PS01-07AM-494
Event Information
Poster Board
PS01-07AM-494
Poster
View posterAbstract
Schizophrenia is a neurodevelopmental disorder in which immune disturbances and gut–brain communication are increasingly recognized as contributing factors. To examine whether intestinal immune changes participate in schizophrenia-relevant phenotypes, we used a maternal immune activation (MIA) mouse model and characterized alterations in the gut immune compartment, with particular attention to intraepithelial lymphocytes (IELs) and local cytokine profiles.
Pregnant dams received lipopolysaccharide at embryonic day 12.5 to induce maternal immune activation. Adult offspring (8 weeks) were assessed for anxiety-like behavior in the Elevated Plus Maze. Intestinal tissues from the small and large bowel were subsequently collected for analysis of IEL subsets and interleukin levels, and immunohistochemistry was performed to visualize CD8⁺ T-cell localization within ileal and colonic epithelium.
MIA offspring exhibited increased anxiety-like behavior compared with controls. These behavioral effects coincided with pronounced changes in IEL composition, including shifts in TCRαβ⁺, CD8αα⁺, CD8αβ⁺, CD4⁺, and TCRγδ⁺CD8αα⁺ populations. Several of these alterations differed between males and females, indicating sex-dependent immune remodeling. Consistent with this, interleukin measurements revealed distinct inflammatory signatures across sexes.
Overall, prenatal immune challenge led to persistent reorganization of intestinal immune networks that paralleled behavioral abnormalities relevant to schizophrenia. Our findings support a role for gut immune dysregulation in shaping neurodevelopmental outcomes and highlight intestinal neuroimmune pathways as potential targets for therapeutic intervention.
Pregnant dams received lipopolysaccharide at embryonic day 12.5 to induce maternal immune activation. Adult offspring (8 weeks) were assessed for anxiety-like behavior in the Elevated Plus Maze. Intestinal tissues from the small and large bowel were subsequently collected for analysis of IEL subsets and interleukin levels, and immunohistochemistry was performed to visualize CD8⁺ T-cell localization within ileal and colonic epithelium.
MIA offspring exhibited increased anxiety-like behavior compared with controls. These behavioral effects coincided with pronounced changes in IEL composition, including shifts in TCRαβ⁺, CD8αα⁺, CD8αβ⁺, CD4⁺, and TCRγδ⁺CD8αα⁺ populations. Several of these alterations differed between males and females, indicating sex-dependent immune remodeling. Consistent with this, interleukin measurements revealed distinct inflammatory signatures across sexes.
Overall, prenatal immune challenge led to persistent reorganization of intestinal immune networks that paralleled behavioral abnormalities relevant to schizophrenia. Our findings support a role for gut immune dysregulation in shaping neurodevelopmental outcomes and highlight intestinal neuroimmune pathways as potential targets for therapeutic intervention.
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