The inflammatory effects of TNF-α and complement component 3 on coagulation
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Date
Authors
Page, Martin J.
Bester, Janette
Pretorius, Etheresia
Journal Title
Journal ISSN
Volume Title
Publisher
Nature Publishing Group
Abstract
Tissue necrosis factor-α (TNF-α) and complement component 3 (C3) are two well-known proinflammatory
molecules. When TNF-α is upregulated, it contributes to changes in coagulation and
causes C3 induction. They both interact with receptors on platelets and erythrocytes (RBCs). Here, we
look at the individual effects of C3 and TNF-α, by adding low levels of the molecules to whole blood
and platelet poor plasma. We used thromboelastography, wide-field microscopy and scanning electron
microscopy to study blood clot formation, as well as structural changes to RBCs and platelets. Clot
formation was significantly different from the naïve sample for both the molecules. Furthermore,
TNF-α exposure to whole blood resulted in platelet clumping and activation and we noted spontaneous
plasma protein dense matted deposits. C3 exposure did not cause platelet aggregation, and only slight
pseudopodia formation was noted. Therefore, although C3 presence has an important function to cause
TNF-α release, it does not necessarily by itself cause platelet activation or RBC damage at these low
concentrations. We conclude by suggesting that our laboratory results can be translated into clinical
practice by incorporating C3 and TNF-α measurements into broad spectrum analysis assays, like
multiplex technology, as a step closer to a patient-orientated, precision medicine approach.
Description
Keywords
Thromboelastography, Laboratory results, Tissue necrosis factor-α (TNF-α), Component 3 (C3), Receptors on platelets and erythrocytes (RBCs)
Sustainable Development Goals
Citation
Page, M.J., Bester, J. & Pretorius, E. 2018, 'The inflammatory effects of TNF-α and complement component 3 on coagulation', Scientific Reports, vol. 8, art. no. 1812, pp. 1-9.