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Published on: August 24, 2019
Experimental appendicitis and appendectomy modulate the CCL20-CCR6 axis to limit inflammatory colitis pathology
1Department of Medicine, St. George Clinical School, University of New South Wales, Sydney, NSW, Australia, rajkumarchel@gmail.com.
Appendicitis and appendectomy (AA) in mice suppresses inflammatory pathways linked to inflammatory bowel diseases (IBD). This finding offers potential new strategies for managing IBD by targeting the CCL20-CCR6 axis and Th17 system.
Area of Science:
- Immunology
- Gastroenterology
Background:
- Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, involve complex interactions between genetics, gut bacteria, and immunity.
- The Th17 cell system and its associated signaling molecules, CCL20 and CCR6, are implicated in IBD pathogenesis.
- Appendicitis and appendectomy (AA) have been observed to prevent or ameliorate human IBD.
Purpose of the Study:
- To investigate the effects of appendectomy on experimental colitis using a novel murine model.
- To explore the molecular mechanisms underlying the protective effects of appendectomy in IBD.
Main Methods:
- A murine model of appendectomy (AA) was established in BALB/c mice.
- Gene expression analysis using microarrays and RT-PCR was performed on colon samples.
- Gene Set Enrichment Analysis (GSEA) was employed to analyze microarray data.
Main Results:
- Prior AA significantly ameliorated experimental colitis in the murine model.
- AA led to a significant suppression of CCL20 expression and Th17 system components in the distal colon.
Conclusions:
- Appendectomy influences key inflammatory pathways, including the CCL20-CCR6 axis and Th17 system, in the context of IBD.
- Targeting these pathways may offer novel therapeutic strategies for managing inflammatory bowel diseases.
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