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To what extent are the terminal stages of sepsis, septic shock, SIRS, and multiple organ dysfunction syndrome actually driven by a prion/amyloid form of fibrin?

Douglas B. Kell, Etheresia Pretorius
doi: https://doi.org/10.1101/057851
Douglas B. Kell
1School of Chemistry, The University of Manchester, 131, Princess St, MANCHESTER M1 7DN, Lancs, UK
2The Manchester Institute of Biotechnology, The University of Manchester, 131, Princess St, MANCHESTER M1 7DN, Lancs, UK
3Centre for Synthetic Biology of Fine and Speciality Chemicals, The University of Manchester, 131, Princess St, MANCHESTER M1 7DN, Lancs, UK
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Etheresia Pretorius
4Department of Physiology, Faculty of Health Sciences, University of Pretoria, Arcadia 0007, South Africa.
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Abstract

A well-established development of increasing disease severity leads from sepsis through septic shock, SIRS, multiple organ dysfunction syndrome and cellular and organismal death. We argue that a chief culprit is the LPS-induced anomalous coagulation of fibrinogen to produce a form of fibrin that is at once inflammatory, resistant to fibrinolysis, and underpins the disseminated intravascular coagulation commonly observed in sepsis. In particular, we argue that the form of fibrin produced is anomalous because much of its normal α-helical content is transformed to β-sheets, as occurs in established amyloidogenic and prion diseases. We hypothesise that these processes play a major role in the passage along the above pathways to organismal death, and that inhibiting them would be of great therapeutic value, a claim for which there is emerging evidence.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted June 10, 2016.
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To what extent are the terminal stages of sepsis, septic shock, SIRS, and multiple organ dysfunction syndrome actually driven by a prion/amyloid form of fibrin?
Douglas B. Kell, Etheresia Pretorius
bioRxiv 057851; doi: https://doi.org/10.1101/057851
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To what extent are the terminal stages of sepsis, septic shock, SIRS, and multiple organ dysfunction syndrome actually driven by a prion/amyloid form of fibrin?
Douglas B. Kell, Etheresia Pretorius
bioRxiv 057851; doi: https://doi.org/10.1101/057851

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