Fibroblast Activation Protein (FAP)-Cleaved Type III Collagen (C3F) is a Potential Marker for Intestinal Fibrosis in Patients with Crohn’s Disease
Introduction
Crohn’s disease (CD) is characterized by chronic inflammation in the gut, where severe complications such as fibrotic strictures require surgical resection. The stricture development involves excessive extracellular matrix (ECM) deposition due to continuous activation of intestinal myofibroblasts, that further contribute to instestinal fibrogenesis. Emerging data suggests that stricture-related intestinal myofibroblasts overexpress a serine protease called fibroblast activation protein (FAP). Furthermore, type III collagen deposition is increased during fibrosis in all layers of the intestinal tract, and studies have shown elevated collagen degradation in serum from patients with CD.
This study aimed to evaluate the potential of FAP-cleaved type III collagen (C3F) as a serum marker for intestinal fibrosis in CD.
Poster
Conclusion
C3F is elevated in patients with stenotic CD compared to luminal CD at baseline and remains elevated after surgical resection, suggesting that C3F reflects fibroblast activity during fibrostenosis and tissue remodeling following surgery. In patients with luminal CD, C3F levels were significantly higher, and early C3F levels (baseline, 3 months and 6 months) were significantly positively associated with ileal stenosis assessed at 12 months. This suggests that increased C3F may be predictive of future endoscopic disease activity or even a potential relapse.
Concluding, the findings of this study highlight the potential use of C3F as a novel biomarker for intestinal fibrosis in CD.
