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


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.
Department of Gastroenterology, Human Nutrition and Internal Diseases, Poznan University of Medical Sciences, Heliodor Swiecicki Hospital, Poznan, Poland. piotr.eder@op.pl.
Piotr
P
Eder
Liliana
L
Lykowska-Szuber
Katarzyna
K
Iwanik
Iwona
I
Krela-Kazmierczak
Kamila
K
Stawczyk-Eder
Przemyslaw
P
Majewski
Krzysztof
K
Linke
Elaine W
EW
Kay
Aldona
A
Wozniak
D000068879:Adalimumab / Q000627:therapeutic use*; D000328:Adult; D043925:Angiogenesis Inducing Agents / Q000627:therapeutic use; D003424:Crohn Disease / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D016099:Endoscopy, Gastrointestinal / Q000379:methods; D005260:Female; D005765:Gastrointestinal Agents / Q000627:therapeutic use; D006801:Humans; D007150:Immunohistochemistry; D000069285:Infliximab / Q000627:therapeutic use*; D007413:Intestinal Mucosa / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D008297:Male; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000276:immunology*; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology
D043925:Angiogenesis Inducing Agents; D005765:Gastrointestinal Agents; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D014409:Tumor Necrosis Factor-alpha; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D000069285:Infliximab; D000068879:Adalimumab
CD31; Crohn’s disease; IHC; VEGF; angiogenesis; anti-TNF therapy