The inflammatory effects of TNF-α and complement component 3 on coagulation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-12

AUTHORS

Martin J. Page, Janette Bester, Etheresia Pretorius

ABSTRACT

Tissue necrosis factor-α (TNF-α) and complement component 3 (C3) are two well-known pro-inflammatory 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. More... »

PAGES

1812

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-018-20220-8

DOI

http://dx.doi.org/10.1038/s41598-018-20220-8

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1100592912

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29379088


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