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

dc.contributor.authorPage, Martin J.en_ZA
dc.contributor.authorBester, Janetteen_ZA
dc.contributor.authorPretorius, Etheresiaen_ZA
dc.date.accessioned2018-03-12T08:06:03Z
dc.date.available2018-03-12T08:06:03Z
dc.date.issued2018
dc.identifier.citationPage, M. J., Bester, J. & Pretorius, E. 2018. The inflammatory effects of TNF-α and complement component 3 on coagulation. Scientific Reports, 8:1812, doi:10.1038/s41598-018-20220-8en_ZA
dc.identifier.issn2045-2322 (Online)
dc.identifier.otherdoi:10.1038/s41598-018-20220-8
dc.identifier.urihttp://hdl.handle.net/10019.1/103221
dc.descriptionCITATION: Page, M. J., Bester, J. & Pretorius, E. 2018. The inflammatory effects of TNF-α and complement component 3 on coagulation. Scientific Reports, 8:1812, doi:10.1038/s41598-018-20220-8.en_ZA
dc.descriptionThe original publication is available at http://www.nature.comen_ZA
dc.descriptionPublication of this article was funded by the Stellenbosch University Open Access Fund.en_ZA
dc.description.abstractTissue 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.en_ZA
dc.description.urihttps://www.nature.com/articles/s41598-018-20220-8
dc.format.extent9 pages : illustrationsen_ZA
dc.language.isoen_ZAen_ZA
dc.publisherNature Publishing Groupen_ZA
dc.subjectCoagulationen_ZA
dc.subjectTissue necrosis factor-α (NTF-α)en_ZA
dc.subjectComplement component 3 (C3)en_ZA
dc.subjectReceptors on platelets and erythrocytes (RBCs)en_ZA
dc.titleThe inflammatory effects of TNF-α and complement component 3 on coagulationen_ZA
dc.typeArticleen_ZA
dc.description.versionPublisher's versionen_ZA
dc.rights.holderAuthors retain copyrighten_ZA


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