Table of Contents Author Guidelines Submit a Manuscript
Journal of Immunology Research
Volume 2015, Article ID 751014, 11 pages
Research Article

Heparin Interaction with the Primed Polymorphonuclear Leukocyte CD11b Induces Apoptosis and Prevents Cell Activation

1Eliachar Research Laboratory, Western Galilee Hospital, 22100 Nahariya, Israel
2Technion Faculty of Medicine, 3525433 Haifa, Israel
3Department of Nephrology and Hypertension, Western Galilee Hospital, 22100 Nahariya, Israel
4Department of Anesthesiology & Critical Care, VA San Diego Healthcare System, San Diego, CA 92161, USA
5Hematology Laboratory, Western Galilee Hospital, 22100 Nahariya, Israel

Received 17 August 2015; Revised 2 November 2015; Accepted 25 November 2015

Academic Editor: Eileen Uribe-Querol

Copyright © 2015 Meital Cohen-Mazor et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Heparin is known to have anti-inflammatory effects, yet the mechanisms are not completely understood. In this study, we tested the hypothesis that heparin has a direct effect on activated polymorphonuclear leukocytes (PMNLs), changing their activation state, and can explain its anti-inflammatory effect. To test our hypothesis, we designed both in vitro and ex vivo studies to elucidate the mechanism by which heparin modulates PMNL functions and therefore the inflammatory response. We specifically tested the hypothesis that priming of PMNLs renders them more susceptible to heparin. Amplified levels of CD11b and increased rate of superoxide release manifested PMNL priming. Increase in cell priming resulted in a dose-dependent increase in heparin binding to PMNLs followed by augmented apoptosis. Blocking antibodies to CD11b inhibited heparin binding and abolished the apoptotic response. Moreover, heparin caused a significant dose-dependent decrease in the rate of superoxide release from PMNLs, which was blunted by blocking antibodies to CD11b. Altogether, this study shows that the interaction of heparin with the PMNL CD11b results in cell apoptosis and explains heparin’s anti-inflammatory effects.