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Updated: Aug 16, 2026

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation
Published on: December 9, 2021
Endothelial cell activation by IL-1beta in the presence of fibrinogen requires alphavbeta3
Abha Sahni1, Sanjeev K Sahni, Charles W Francis
1Department of Medicine, University of Rochester School of Medicine & Dentistry, Rochester, NY, USA. Abha_Sahni@urmc.rochester.edu
Objective:
The purpose of this study was to investigate the receptor requirements for enhanced IL-1beta-induced secretion of nitric oxide (NO) by endothelial cells (ECs) in the presence of fibrinogen.
Methods And Results:
ECs were exposed to IL-1beta with or without fibrinogen and NO was measured as nitrite. NO production by EC exposed to fibrinogen (0.3+/-0.1 micromol/L) was comparable concentration to control (0.2+/-0.1 micromol/L), but IL-1beta significantly increased NO production (0.8+/-0.1 micromol/L), and the combination of both fibrinogen and IL-1beta resulted in a further increase to 2.2+/-0.2 micromol/L (P<0.002). 7E3 or LM609, antibodies to alphavbeta3, inhibited NO production stimulated by fibrinogen-bound IL-1beta to 0.2+/-0.1 micromol/L (P<0.001) or 0.2+/-0.03 micromol/L (P<0.0001), respectively. These levels were comparable to control and significantly less than with IL-1beta (P<0.002). EC or fibroblasts exposed to both fibrinogen and IL-1beta, but not vitronectin and IL-1beta, demonstrated positive Western blotting for alphavbeta3 after immunopurification with anti- IL-1R, indicating specific association between alphavbeta3 and IL-1R. Dual immunofluorescence also revealed colocalization of alphavbeta3 and IL-1R only when the cells were exposed to both fibrinogen and IL-1beta.
Conclusions:
The enhanced NO production by ECs in the presence of fibrinogen-bound IL-1beta requires the coordinated effects of colocalized alphavbeta3 and IL-1R.
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