Soluble selectins, sICAM, sVCAM, and angiogenic proteins in different activity groups of patients with inflammatory bowel disease.
The endothelium is involved in the pathogenesis of inflammatory bowel disease (IBD). So far knowledge of the precise role of soluble adhesion molecules and angiogenic factors at different periods of activity in IBD is scarce or contradictory. Our goal in this study was to determine the serum levels of adhesion molecules and angiogenic factors in IBD patients at different periods of disease activity--clinical remission, biochemical evidence of inflammation, and clinical evidence of activity. We used a cross-sectional study design consisting of 218 patients (145 with Crohn's disease [CD] and 73 with ulcerative colitis [UC]) and 115 randomly assymptomatic blood donors. To assess disease activity, Harvey and Bradshaw's and Truelove-Witts' indexes were used. Circulating plasma sE-selectin (sE-S), sP-selectin (sP-S), human soluble vascular cell adhesion molecule-1 (sVCAM-1), and human soluble intercellular adhesion molecule-1 (sICAM-1) and serum levels of human vascular endothelial growth factor (VEGF), angiogenin (ANG), and placenta growth factor (P/GF) were measured with ELISAs. The amount of mRNA VEGF in blood mononuclear cells was also evaluated. In inactive CD patients, serum levels of sP-S, sE-S, sVCAM, and sICAM were significantly lower (P < 0.05) than in controls. In active CD patients, only the sE-S values were higher than in controls. In UC patients, sP-S and sVCAM levels were significantly lower than those in controls. Considering growth factors, CD patients in remission had levels of ANG and VEGF lower than those found in controls. The VEGF RNAm in blood mononuclear cells was similar among all CD activity groups. In conclusion, in UC patients the serum levels of VEGF, ANG, and P/GF were similar to those in controls. The serum levels of adhesion molecules and angiogenic factors were low in IBD patients in periods of remission. Low levels of angiogenic factors in inactive CD patients suggest dysfunction of the angiogenic process and wound repair.
Magro
F
F
Gastroenterology Unit, Hospital S. João, Porto, Portugal. fm@med.up.pt
Araujo
F
F
Pereira
P
P
Meireles
E
E
Diniz-Ribeiro
M
M
Velosom
F Tavarela
FT
D000293:Adolescent; D000328:Adult; D042501:Angiogenic Proteins / Q000097:blood; D015415:Biomarkers / Q000097:blood*; D015815:Cell Adhesion Molecules / Q000097:blood*; D003093:Colitis, Ulcerative / Q000097:blood*; D003424:Crohn Disease / Q000097:blood*; D003430:Cross-Sectional Studies; D019040:E-Selectin / Q000097:blood; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood; D000072483:Placenta Growth Factor; D011257:Pregnancy Proteins / Q000097:blood; D012995:Solubility; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
D042501:Angiogenic Proteins; D015415:Biomarkers; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D019007:P-Selectin; C000608036:PGF protein, human; D011257:Pregnancy Proteins; D019010:Vascular Cell Adhesion Molecule-1; D042461:Vascular Endothelial Growth Factor A; D018799:Intercellular Adhesion Molecule-1; D000072483:Placenta Growth Factor