Related Experiment Video
Updated: Aug 19, 2026

Controlled Microfluidic Environment for Dynamic Investigation of Red Blood Cell Aggregation
Published on: June 4, 2015
Inflammation-sensitive proteins and erythrocyte aggregation in atherothrombosis
Einor Ben Assayag1, Nathan Bornstein, Itzhak Shapira
1Department of Internal Medicine D, Tel-Aviv Sourasky Medical Center, and Sackler Faculty of Medicine, 6 Weizman Street, Tel Aviv University, Tel Aviv 64239, Israel.
Objective:
To find the relative contribution of various inflammation-sensitive proteins including fibrinogen, immunoglobulins (IgG, IgM and IgA), ceruloplasmin and high sensitivity C-reactive protein (hs-CRP) to the induction and/or maintenance of enhanced erythrocyte adhesiveness/aggregation in the peripheral blood of individuals with atherothrombotic risk factors.
Methods:
The degree of erythrocyte adhesiveness/aggregation was determined by a simple slide test and image analysis. In addition, we measured various inflammation-sensitive protein levels including fibrinogen, ceruloplasmin, immunoglobulins and hs-CRP in a group of 234 individuals with atherothrombotic risk factors and healthy ones. Pearson partial correlations and multiple linear regression analysis were performed.
Results:
Fibrinogen was found to be the major protein contributing to the enhanced erythrocyte adhesiveness/aggregation, explaining 30% of the model. Fibrinogen and IgG together explained 32.4% of the model. Other inflammation-sensitive proteins did not reach statistical significance and were excluded from the model.
Conclusions:
Among inflammation-sensitive proteins measured in our cohort, fibrinogen is the dominant contributor to erythrocyte adhesiveness/aggregation in the peripheral blood of individuals with atherothrombotic risk factors and healthy ones. These findings may pave the way for the development of therapeutic strategies directed at the attenuation of erythrocyte aggregability in individuals with atherothrombosis.
Related Concept Videos
Inflammation
Atherosclerosis I: Introduction
Acute Inflammation III: Local and Systemic Effects
Coronary Artery Disease II: Pathophysiology
Acute Inflammation I: Inflammatory Response
Anticoagulant Drugs: Low-Molecular-Weight Heparins