作者: Peter K. Henke , Lisa A. DeBrunye , Robert M. Strieter , Jonathan S. Bromberg , Martin Prince
DOI: 10.4049/JIMMUNOL.164.4.2131
关键词:
摘要: Post-thrombotic inflammation probably contributes to chronic venous insufficiency, and little effective treatment exists. IL-10 is an anti-inflammatory cytokine that previously has been shown decrease perithrombotic thrombosis. We investigated in a rat model whether local expression of viral (vIL-10) segment vein undergoes thrombosis would confer effect how this might be mediated. Rats underwent inferior vena cava isolation, cannulation, instillation saline or adenovirus encoding either beta-galactosidase vIL-10. Two days after transfection, was induced, 2 the rats gadolinium (Gd)-enhanced magnetic resonance venography exam, segments were harvested. Tissue transfection confirmed by RT-PCR vIL-10 positive 5-bromo-4-chloro-3-indolyl beta-d-galactopyranoside (X-Gal) staining. significantly decreased both leukocyte wall extravasation area Gd enhancement compared with those controls, suggesting inflammation. Immunohistochemistry demonstrated endothelial border staining P- E-selectin, while ELISA tissue homogenates revealed E-selectin ICAM-1 levels group controls. Importantly, native cellular not different between groups. However, neither clot weight nor coagulation indexes, including factor activity, Ag, von Willebrand levels, affected expression. These data suggest decreases thrombosis-associated cell adhesion molecule expression, but does directly affect procoagulant activity.