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Experimental colitis reduces microglial cell activation in the mouse brain without affecting microglial cell numbers
Hoda M Sroor1,2, Ahmed M Hassan1, Geraldine Zenz1
1Research Unit of Translational Neurogastroenterology, Division of Pharmacology, Otto Loewi Research Centre for Vascular Biology, Immunology and Inflammation, Medical University of Graz, Graz, Austria.
Scientific Reports
|December 29, 2019
Summary
Inflammatory bowel disease (IBD) causes changes in brain immune cells called microglia. This study shows colitis alters microglial function in the brain, potentially linking gut inflammation to mental health.
Area of Science:
- Neuroscience
- Immunology
- Gastroenterology
Background:
- Inflammatory bowel disease (IBD) is linked to psychiatric disorders, suggesting gut-brain axis dysfunction.
- Microglia, the brain's immune cells, are implicated in mental health but their role in IBD is unclear.
Purpose of the Study:
- To investigate if dextran sulphate sodium (DSS)-induced colitis alters microglial phenotypes in the brain.
- To explore the connection between gastrointestinal inflammation and brain immune cell activity.
Main Methods:
- Utilized a DSS-induced colitis mouse model.
- Assessed microglial activation markers (Iba-1, CD68) via immunoreactivity in specific brain regions.
- Employed flow cytometry to analyze macrophage populations.
- Conducted gene expression analysis of microglial markers in the medial prefrontal cortex (mPFC).
Main Results:
- Colitis reduced Iba-1 and CD68 immunoreactivity in the mPFC, but not all brain regions.
- Observed an increase in monocyte-derived macrophages during colitis.
- Gene expression in the mPFC indicated both M1 and M2 microglial activation states.
Conclusions:
- Experimental colitis alters microglial function in the brain.
- Inflammation associated with IBD may propagate to the central nervous system, affecting brain immune cells.
