| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Pathology, LSU Health Sciences Center-Shreveport, Shreveport, LA, USA
2 Department of Molecular and Cellular Physiology, LSU Health Sciences Center-Shreveport, Shreveport, LA, USA
3 Department of Pharmaceutical Chemistry, University of Kansas, Lawrence, KS, USA
4 Department of Pathology, LSU Health Sciences Center-Shreveport, Shreveport, LA, USA; Department of Molecular and Cellular Physiology, LSU Health Sciences Center-Shreveport, Shreveport, LA, USA
* To whom correspondence should be addressed. E-mail: ckevil{at}lsuhsc.edu.
Inflammatory Bowel Disease (IBD) is a chronic inflammatory disorder characterized by increased leukocyte recruitment and subsequent tissue damage. An increase in the density of the microvasculature of the colon during IBD has been suggested, leading to the concept that angiogenesis may play a pathological role in IBD. Increased tissue and serum levels of the angiogenic cytokine VEGF-A have been reported in cases of active IBD. Here, we examine the hypothesis that VEGF-A exerts a pro-inflammatory effect on colon microvascular endothelium that contributes to colonic inflammation. Leukocyte adhesion to VEGF-A stimulated colon microvascular endothelial cells was examined using a parallel plate hydrodynamic flow chamber. ICAM-1 adhesion molecule expression on colonic microvascular endothelium was also determined in response to VEGF-A stimulation, along with characterization of leukocyte adhesion molecule expression. High dose VEGF-A (50 ng/ml) stimulation increased neutrophil and T cell adhesion to and decreased rolling velocities on activated endothelium, whereas low dose VEGF-A (10 ng/ml) was without effect. Colonic endothelium constitutively expressed ICAM-1, which was significantly increased by treatment with 50 ng/ml VEGF-A or 10 ng/ml of TNF-
but not 10 ng/ml VEGF-A. T cells expressed CD18 and CD11a, with no expression of CD11b; whereas, neutrophils expressed CD18, CD11a, and CD11b. Lastly, VEGF-A dependent leukocyte adhesion was found to occur in a CD18 dependent manner. These results demonstrate that VEGF-A levels found in IBD exerts a pro-inflammatory effect similar to other inflammatory agents and suggests that this cytokine may serve as an intermediary between angiogenic stimulation and cell mediated immune responses.
This article has been cited by other articles:
|
|
 |
|
  B. P. Cheppudira, B. M. Girard, S. E. Malley, K. C. Schutz, V. May, and M. A. Vizzard Upregulation of vascular endothelial growth factor isoform VEGF-164 and receptors (VEGFR-2, Npn-1, and Npn-2) in rats with cyclophosphamide-induced cystitis Am J Physiol Renal Physiol, September 1, 2008; 295(3): F826 - F836. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Deban, C. Correale, S. Vetrano, A. Malesci, and S. Danese Multiple Pathogenic Roles of Microvasculature in Inflammatory Bowel Disease: A Jack of All Trades Am. J. Pathol., June 1, 2008; 172(6): 1457 - 1466. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. D. Sharp, M. Huang, J. Glawe, D. R. Patrick, S. Pardue, S. C. Barlow, and C. G. Kevil Stromal Cell Derived Factor-1/CXCL12 Stimulates Chemorepulsion of NOD/LtJ T-Cell Adhesion to Islet Microvascular Endothelium Diabetes, January 1, 2008; 57(1): 102 - 112. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. H. Chidlow Jr., D. Shukla, M. B. Grisham, and C. G. Kevil Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues Am J Physiol Gastrointest Liver Physiol, July 1, 2007; 293(1): G5 - G18. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
