The influence of anti-TNF therapy on CD31 and VEGF expression in colonic mucosa of Crohn's disease patients in relation to mucosal healing

Folia Histochem Cytobiol. 2016;54(2):75-80. doi: 10.5603/FHC.a2016.0008. Epub 2016 Jun 8.

Abstract

Introduction: Immune-mediated angiogenesis may play an important role in the pathogenesis of inflammatory lesions in Crohn's disease (CD). The study aimed to assess the influence of anti-tumour necrosis factor (anti-TNF) therapy on the angiogenesis in relation to microscopic and endoscopic healing in CD patients.

Material and methods: Colonic tissue samples from 17 CD patients were taken during colonoscopy before and after anti-TNF therapy. Endoscopic and microscopic severities were estimated using validated scores. Immunohistochemical expression of CD31 and vascular endothelial growth factor (VEGF) were assessed in parallel.

Results: The expression of CD31 and VEGF decreased significantly after the anti-TNF therapy in parallel to endoscopic improvement; however, the microscopic activity did not change significantly. There was a correlation between the change in CD31 and VEGF expression (p = 0.01; r = 0.6), as well as endoscopic healing (p = 0.04; r = 0.4). CD31 immunoexpression correlated with the number of poly- and mononuclear cells in the infiltrates in the mucosal lamina propria before the therapy (p = 0.02; r = 0.5).

Conclusions: We suggest that modulation of vascular proliferation can be a novel option to increase the efficacy of biological therapy in CD.

Keywords: CD31; Crohn’s disease; IHC; VEGF; angiogenesis; anti-TNF therapy.

MeSH terms

  • Adalimumab / therapeutic use*
  • Adult
  • Angiogenesis Inducing Agents / therapeutic use
  • Crohn Disease / drug therapy*
  • Crohn Disease / metabolism
  • Crohn Disease / pathology
  • Endoscopy, Gastrointestinal / methods
  • Female
  • Gastrointestinal Agents / therapeutic use
  • Humans
  • Immunohistochemistry
  • Infliximab / therapeutic use*
  • Intestinal Mucosa / blood supply
  • Intestinal Mucosa / drug effects
  • Intestinal Mucosa / metabolism*
  • Intestinal Mucosa / pathology
  • Male
  • Platelet Endothelial Cell Adhesion Molecule-1 / biosynthesis*
  • Platelet Endothelial Cell Adhesion Molecule-1 / genetics
  • Platelet Endothelial Cell Adhesion Molecule-1 / immunology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / immunology*
  • Vascular Endothelial Growth Factor A / biosynthesis*
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor A / immunology

Substances

  • Angiogenesis Inducing Agents
  • Gastrointestinal Agents
  • Platelet Endothelial Cell Adhesion Molecule-1
  • Tumor Necrosis Factor-alpha
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • Infliximab
  • Adalimumab