ArticleFrontiers in immunology2026
The exosomal miR-26b-3p derived from Crohn's disease-associated mesenteric adipose tissue induces M1 macrophage polarization and exacerbates ileocolonic anastomosis inflammation via the p38-MAPK signaling pathway.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Advances in understanding exosome-mediated regulation of macrophage function.Frontiers in immunology · 2026Review
- Macrophage dysregulation in inflammatory bowel disease: cellular heterogeneity, pathogenic mechanism, and treatment.Frontiers in immunology · 2026Review
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Authors and funding
8 authors.
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Abstract
Purpose: Crohn's Disease (CD) is a chronic inflammatory condition characterized by intestinal inflammation, especially in the progression of postoperative anastomotic recurrence. Recent evidence implicates mesenteric adipose tissue (MAT) in CD pathogenesis, particularly through its exosome secretion, which may influence inflammation pathways. The molecular mechanisms driving this inflammation remain inadequately understood. Methods: Exosomes were isolated from MAT of the diseased bowel and macroscopically normal MAT from the surgical margins of patients with CD. We induced chronic intestinal inflammation in mice using dinitrobenzene sulfonic acid (DNBS), simulating CD-like MAT. Using a surgical model of IL10-knockout mice, we performed a series of experiments Results: Hypertrophic MAT-Exosomes (Ht-exos) promoted ileocolonic anastomotic inflammation by activating macrophage M1 polarization in CD. Conclusion: Our findings reveal that exosomal miR-26b-3p drives widespread macrophage inflammation and M1 polarization in hypertrophic MAT-induced ileocolonic anastomosis inflammation via the MAPK pathway.
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