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Background <p>Fibrostenotic stricturing disease affects 30–50% of patients with Crohn’s disease (CD), leading to intestinal resection. Currently, there exists a great medical need to identify biomarkers related to fibrostenotic strictures for optimized patient management. Thus, we investigated PRO-C16 as a biomarker for intestinal fibrosis in patients with CD.</p> Methods <p>Human serum from two independent cohorts of CD patients (cohort 1: <i>n</i> = 44, cohort 2: <i>n</i> = 52), healthy subjects (<i>n</i> = 37), and serum from a chronic rat dextran sodium sulfate (DSS) colitis model were included. The Montreal classification for CD disease behavior was applied for patient phenotyping.</p> Results <p>PRO-C16 was elevated in patients with CD compared to healthy donors (<i>P</i> &lt; 0.001), and in CD patients with fibrostenotic strictures in both cohorts. Furthermore, PRO-C16 was able to separate CD patients with strictures(B2) from CD patients without strictures (B1 and B3) (Cohort 1 [<i>P</i> &lt; 0.01, AUC:0.75], and Cohort 2 [<i>P</i> &lt; 0.05, AUC:0.71). In the chronic DSS rat colitis model, PRO-C16 was elevated after the second and fourth cycles of DSS, reflecting collagen deposition in that model.</p> Conclusion <p>The biomarker PRO-C16 was associated with a stricturing disease phenotype, indicating that PRO-C16 may be a potential marker of intestinal fibrosis in CD, with the potential to aid in the clinical development of novel stromal-immune therapeutic agents.</p>

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Serological assessment of PRO-C16 (type XVI collagen formation) reflects intestinal fibrostenotic strictures in patients with crohn’s disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月8日

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  • Joachim H. Mortensen,
  • M. Lindholm,
  • L. Langholm,
  • P. Giuffrida,
  • D. Ruane,
  • T. Manon-Jensen,
  • G. Mazza,
  • F. Caprioli,
  • L. Pastorelli,
  • A-C. Bay-Jensen,
  • M. Pinzani,
  • M. A. Karsdal,
  • A. Di Sabatino

摘要

Background

Fibrostenotic stricturing disease affects 30–50% of patients with Crohn’s disease (CD), leading to intestinal resection. Currently, there exists a great medical need to identify biomarkers related to fibrostenotic strictures for optimized patient management. Thus, we investigated PRO-C16 as a biomarker for intestinal fibrosis in patients with CD.

Methods

Human serum from two independent cohorts of CD patients (cohort 1: n = 44, cohort 2: n = 52), healthy subjects (n = 37), and serum from a chronic rat dextran sodium sulfate (DSS) colitis model were included. The Montreal classification for CD disease behavior was applied for patient phenotyping.

Results

PRO-C16 was elevated in patients with CD compared to healthy donors (P < 0.001), and in CD patients with fibrostenotic strictures in both cohorts. Furthermore, PRO-C16 was able to separate CD patients with strictures(B2) from CD patients without strictures (B1 and B3) (Cohort 1 [P < 0.01, AUC:0.75], and Cohort 2 [P < 0.05, AUC:0.71). In the chronic DSS rat colitis model, PRO-C16 was elevated after the second and fourth cycles of DSS, reflecting collagen deposition in that model.

Conclusion

The biomarker PRO-C16 was associated with a stricturing disease phenotype, indicating that PRO-C16 may be a potential marker of intestinal fibrosis in CD, with the potential to aid in the clinical development of novel stromal-immune therapeutic agents.