Dynamical modeling of TNF-α, IL-6, and IL-10 interactions in stroke-induced inflammation.

ABSTRACT: In acute stroke, dysregulated cytokine interactions drive secondary injury, yet bidirectional feedback mechanisms between pro-inflammatory mediators (TNF-α, IL-6) and the anti-inflammatory mediator IL-10 remain poorly quantified. We developed a systems biology model using nonlinear ordinary differential equations (ODEs) to resolve these dynamics, incorporating Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB)-mediated cross-activation, delayed IL-10 induction via a Hill function, and empirical parameterization from stroke data. Mathematical analysis revealed bistable inflammatory states via bifurcation theory, mechanistically explaining divergent inflammatory trajectory. Steady-state and stability analyses identified a critical IL-10 suppression threshold ([Formula: se

SUBMITTER: Arishi FAM 

PROVIDER: S-EPMC12818665 | biostudies-literature | 2026

REPOSITORIES: biostudies-literature