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Investigating Intestinal Inflammation in DSS-induced Model of IBD
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Cortical Inflammation is Increased in a DSS-Induced Colitis Mouse Model.

Ying Han1,2, Tong Zhao2, Xiang Cheng2

  • 1Center for Brain Disorders Research, Capital Medical University, Beijing Institute of Brain Disorders, Beijing, 100069, China.

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|September 19, 2018
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Summary

Inflammatory bowel disease (IBD) can cause brain dysfunction. This study shows dextran sodium sulfate (DSS)-induced colitis increases systemic inflammation, leading to cortical inflammation and microglial activation in mice.

Keywords:
Blood-brain barrierColitisCortical inflammationDextran sodium sulfateEndotoxin

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Area of Science:

  • Neuroinflammation
  • Gastroenterology
  • Immunology

Background:

  • Inflammatory bowel disease (IBD) is linked to brain dysfunction, but mechanisms are unclear.
  • Systemic inflammation from IBD may affect the central nervous system.

Purpose of the Study:

  • To investigate the impact of dextran sodium sulfate (DSS)-induced colitis on cortical inflammation.
  • To explore the relationship between colitis, systemic inflammation, and brain changes.

Main Methods:

  • Mice were administered 5% DSS in drinking water for 7 days.
  • Serum and cortical tissue cytokine levels (IL-6, TNF-α) were measured.
  • Endotoxin levels, microglial activation, and tight junction protein expression (occludin, claudin-5) in the brain were assessed.

Main Results:

  • DSS-induced colitis significantly increased serum IL-6 and cortical IL-6/TNF-α levels.
  • Microglial cells in the brain showed significant activation.
  • Expression of occludin and claudin-5 was reduced in brain tissue.
  • Endotoxin levels showed a non-significant increasing trend.

Conclusions:

  • DSS-induced colitis exacerbates systemic inflammation, leading to cortical inflammation.
  • Up-regulation of serum cytokines plays a role in transmitting inflammation to the brain.
  • Colitis impacts brain tissue by activating microglia and altering tight junction proteins.