Subclinical gut inflammation in spondyloarthritis is associated with a pro-angiogenic intestinal mucosal phenotype
(2011) ANNALS OF THE RHEUMATIC DISEASES. 70(11). p.2044-2048- abstract
- Background Vascular endothelial growth factor (VEGF-A) and placental growth factor (PlGF) are major regulators of pathological angiogenesis, which is a prominent feature of both Crohn's disease (CD) and peripheral synovitis in spondyloarthritis. Objective To investigate the presence of VEGF-A and PlGF in the gut of spondyloarthritis patients and to link this finding with subclinical gut inflammation in these patients. Methods Intestinal biopsies from healthy controls, CD patients, spondyloarthritis patients with or without subclinical gut inflammation and rheumatoid arthritis (RA) patients were stained for VEGF-A, PlGF, CD31 and vascular cell adhesion molecule 1 (VCAM-1) and digitally analysed. Results Spondyloarthritis patients with subclinical gut inflammation had markedly increased intestinal VEGF-A expression (p<0.001), mucosal vascularisation (p<0.001) and VCAM-1 expression (p<0.01) compared with healthy controls and RA patients, which, unlike in CD patients, was also seen when the gut inflammation was in a quiescent state. PlGF expression was highly increased in the subclinically inflamed gut of spondyloarthritis (p<0.01 compared with healthy controls), but not at all in CD. Conclusion A pro-angiogenic intestinal phenotype is observed in spondyloarthritis patients with quiescent chronic gut inflammation. This favours an environment for enhanced trafficking of immune cells in this subpopulation.
Please use this url to cite or link to this publication:
http://hdl.handle.net/1854/LU-1854164
- author
- Pieter Hindryckx UGent, Debby Laukens UGent, Gerlinde Serry, Liesbet Van Praet, Claude Cuvelier, Herman Mielants, Harald Peeters UGent, Dirk Elewaut UGent and Martine De Vos UGent
- organization
- year
- 2011
- type
- journalArticle (original)
- publication status
- published
- subject
- keyword
- ENDOTHELIAL GROWTH-FACTOR, BOWEL-DISEASE PATHOGENESIS, ANKYLOSING-SPONDYLITIS, EXPRESSION, ARTHRITIS, CRITERIA, CELLS, VEGF
- journal title
- ANNALS OF THE RHEUMATIC DISEASES
- Ann. Rheum. Dis.
- volume
- 70
- issue
- 11
- pages
- 2044 - 2048
- Web of Science type
- Article
- Web of Science id
- 000295399700028
- JCR category
- RHEUMATOLOGY
- JCR impact factor
- 8.727 (2011)
- JCR rank
- 1/29 (2011)
- JCR quartile
- 1 (2011)
- ISSN
- 0003-4967
- DOI
- 10.1136/ard.2010.149229
- project
- Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
- language
- English
- UGent publication?
- yes
- classification
- A1
- copyright statement
- I have transferred the copyright for this publication to the publisher
- id
- 1854164
- handle
- http://hdl.handle.net/1854/LU-1854164
- date created
- 2011-07-06 17:06:03
- date last changed
- 2016-12-19 15:42:17
@article{1854164, abstract = {Background Vascular endothelial growth factor (VEGF-A) and placental growth factor (PlGF) are major regulators of pathological angiogenesis, which is a prominent feature of both Crohn's disease (CD) and peripheral synovitis in spondyloarthritis. Objective To investigate the presence of VEGF-A and PlGF in the gut of spondyloarthritis patients and to link this finding with subclinical gut inflammation in these patients. Methods Intestinal biopsies from healthy controls, CD patients, spondyloarthritis patients with or without subclinical gut inflammation and rheumatoid arthritis (RA) patients were stained for VEGF-A, PlGF, CD31 and vascular cell adhesion molecule 1 (VCAM-1) and digitally analysed. Results Spondyloarthritis patients with subclinical gut inflammation had markedly increased intestinal VEGF-A expression (p{\textlangle}0.001), mucosal vascularisation (p{\textlangle}0.001) and VCAM-1 expression (p{\textlangle}0.01) compared with healthy controls and RA patients, which, unlike in CD patients, was also seen when the gut inflammation was in a quiescent state. PlGF expression was highly increased in the subclinically inflamed gut of spondyloarthritis (p{\textlangle}0.01 compared with healthy controls), but not at all in CD. Conclusion A pro-angiogenic intestinal phenotype is observed in spondyloarthritis patients with quiescent chronic gut inflammation. This favours an environment for enhanced trafficking of immune cells in this subpopulation.}, author = {Hindryckx, Pieter and Laukens, Debby and Serry, Gerlinde and Van Praet, Liesbet and Cuvelier, Claude and Mielants, Herman and Peeters, Harald and Elewaut, Dirk and De Vos, Martine}, issn = {0003-4967}, journal = {ANNALS OF THE RHEUMATIC DISEASES}, keyword = {ENDOTHELIAL GROWTH-FACTOR,BOWEL-DISEASE PATHOGENESIS,ANKYLOSING-SPONDYLITIS,EXPRESSION,ARTHRITIS,CRITERIA,CELLS,VEGF}, language = {eng}, number = {11}, pages = {2044--2048}, title = {Subclinical gut inflammation in spondyloarthritis is associated with a pro-angiogenic intestinal mucosal phenotype}, url = {http://dx.doi.org/10.1136/ard.2010.149229}, volume = {70}, year = {2011}, }
- Chicago
- HINDRYCKX, PIETER, Debby Laukens, Gerlinde Serry, Liesbet Van Praet, Claude Cuvelier, Herman Mielants, Harald Peeters, Dirk Elewaut, and Martine De Vos. 2011. “Subclinical Gut Inflammation in Spondyloarthritis Is Associated with a Pro-angiogenic Intestinal Mucosal Phenotype.” Annals of the Rheumatic Diseases 70 (11): 2044–2048.
- APA
- HINDRYCKX, P., Laukens, D., Serry, G., Van Praet, L., Cuvelier, C., Mielants, H., Peeters, H., et al. (2011). Subclinical gut inflammation in spondyloarthritis is associated with a pro-angiogenic intestinal mucosal phenotype. ANNALS OF THE RHEUMATIC DISEASES, 70(11), 2044–2048.
- Vancouver
- 1.HINDRYCKX P, Laukens D, Serry G, Van Praet L, Cuvelier C, Mielants H, et al. Subclinical gut inflammation in spondyloarthritis is associated with a pro-angiogenic intestinal mucosal phenotype. ANNALS OF THE RHEUMATIC DISEASES. 2011;70(11):2044–8.
- MLA
- HINDRYCKX, PIETER, Debby Laukens, Gerlinde Serry, et al. “Subclinical Gut Inflammation in Spondyloarthritis Is Associated with a Pro-angiogenic Intestinal Mucosal Phenotype.” ANNALS OF THE RHEUMATIC DISEASES 70.11 (2011): 2044–2048. Print.