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Modeling of the effects of IL-17 and TNF-α on endothelial cells and thrombus growth

Anass Bouchnita1, Pierre Miossec2, Alen Tosenberger3

  • 1Laboratoire de biométrie et biologie évolutive (LBBE), UMR 5558 CNRS, Université Lyon-1, 69376 Lyon, France; Mohammadia School of Engineering (EMI), Université Mohammed-V, 10080 Rabat, Morocco.

Comptes Rendus Biologies
|December 3, 2017
PubMed

Insights

Cytokines Tumor Necrosis Factor-alpha (TNF-α) and Interleukin-17 (IL-17) contribute to cardiovascular events in inflammatory diseases. Mathematical models show these cytokines can cause thrombosis by promoting blood coagulation and clot growth.

Area of Science:

  • Rheumatology
  • Cardiovascular Medicine
  • Computational Biology

Background:

  • Rheumatoid and psoriatic arthritis are chronic inflammatory conditions associated with increased cardiovascular events (CVE).
  • Cytokines Tumor Necrosis Factor-alpha (TNF-α) and Interleukin-17 (IL-17) play a role in the pathogenesis of these diseases and cardiovascular complications.
  • Previous research indicates that combined TNF-α and IL-17 promote procoagulation, reduce anticoagulation, and increase platelet aggregation, potentially leading to thrombosis.

Purpose of the Study:

  • To develop mathematical models and perform numerical simulations of blood coagulation and clot growth.
  • To investigate the influence of TNF-α and IL-17 on thrombosis development.
  • To explore the conditions under which these cytokines can cause partial or complete occlusion of blood vessels.

Main Methods:

  • Mathematical modeling of blood coagulation and clot growth.
  • Numerical simulations to analyze the effects of TNF-α and IL-17.
  • Development of approximate analytical models to complement simulations.

Main Results:

  • Demonstrated that TNF-α and IL-17 can provoke thrombosis, leading to blood vessel occlusion.
  • Identified specific regimes of blood coagulation and conditions conducive to occlusion under the influence of these cytokines.
  • Mathematical models successfully predict thrombosis development in a patient-specific manner.

Conclusions:

  • The combined action of TNF-α and IL-17 significantly contributes to thrombosis in the context of chronic inflammatory diseases.
  • Mathematical modeling provides a powerful tool for understanding the mechanisms of cytokine-induced thrombosis.
  • These findings have implications for predicting and potentially managing cardiovascular risk in patients with inflammatory arthritis.

Keywords:
Mathematical modelingModélisation mathématiquePolyarthrites psoriasquesPolyarthrites rhumatoïdesPsoriatic arthritisRheumatoid arthritisTNF and IL-17TNF et IL-17ThromboseThrombosis

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