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Infliximab therapy downregulation of basic fibroblast growth factor/syndecan 1 link: a possible molecular pathway of mucosal healing in ulcerative colitis
  1. Enzo Ierardi1,
  2. Floriana Giorgio1,
  3. Mariangela Zotti1,
  4. Rosa Rosania1,
  5. Mariabeatrice Principi2,
  6. Stefania Marangi3,
  7. Nicola Della Valle1,
  8. Vincenzo De Francesco1,
  9. Alfredo Di Leo2,
  10. Marcello Ingrosso3,
  11. Carmine Panella1
  1. 1Section of Gastroenterology, Department of Medical Sciences, University of Foggia, Foggia, Italy
  2. 2Section of Gastroenterology, Department of Emergency and Organ Transplantation, University of Bari, Bari, Italy
  3. 3Section of Biotechnology, ‘Sacro Cuore’ University of Campobasso, Campobasso, Italy
  1. Correspondence to Professor Enzo Ierardi, Gastroenterology Section, Department of Medical Sciences, University of Foggia, AOU Ospedali Riuniti, Viale Pinto, 71100 Foggia, Italy; enzo.ierardi{at}


Background It is known that syndecan 1 in inflammatory bowel diseases is able to migrate from epithelial basolateral site to the stromal area and apical surface of epithelium with a consequent activation and modulation of basic fibroblast growth factor (bFGF), and this process sustains mucosal healing of ulcers. On the other hand, tumour necrosis factor (TNF) α mucosal levels are directly related to the entity of the damage in these disorders.

Aim of the study A ‘post-hoc’ retrospective study was performed to estimate mucosal TNF α in rectal biopsies of subjects with ulcerative colitis (UC) before and after effective infliximab therapy and its relationship with syndecan 1, bFGF and endoscopic mucosal healing.

Material and methods Paraffin-embedded rectal samples from 12 patients with UC responders to infliximab were analysed for TNF α, syndecan 1 and bFGF before and 6 months after therapy using a real-time reverse transcriptase polymersase chain reaction. Additionally, syndecan 1 location was evaluated by immunohistochemistry. Samples from 12 subjects with irritable bowel symptoms without endoscopic/histological abnormalities represented the control group. Mucosal healing induced by the treatment was defined by an endoscopic Mayo subscore changing from 2–3 to 0. ANOVA plus Student–Newman–Keuls was used for statistical analysis.

Results The authors found that in the active disease, an increase in TNF α (p<0.001) is accompanied by raised levels of both syndecan 1 (p<0.005) and bFGF (p<0.005) compared with the control group. Infliximab-induced TNF α decrease to levels similar to controls is associated with both endoscopic mucosal healing and adhesion molecule/growth factor significant reduction. Additionally, syndecan 1 location, which is predominant in the stromal cells and apical epithelium in the active disorder, is quite exclusively located at the basolateral epithelial area in both healed mucosa and controls.

Conclusions Balanced interaction among TNF α inhibition by infliximab, syndecan 1 migration, bFGF repair modulation and final adhesion molecule reversal to its normal location might represent a suitable molecular pathway of endoscopic mucosal healing in UC.

  • Ulcerative colitis
  • syndecan 1
  • basic fibroblast growth factor
  • tumour necrosis factor
  • cell adhesion molecules
  • cytokines
  • gastrointestinal disease
  • inflammatory bowel disease
  • PCR

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  • Funding Italian University and Research Ministry.

  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.