ArticlePloS one2026
Dynamical modeling of TNF-α, IL-6, and IL-10 interactions in stroke-induced inflammation.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Effects of surgical timing on inflammatory responses, oxidative stress, and immune modulation in Wagyu calves following castration.BMC veterinary research · 2026Article
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Authors and funding
3 authors.
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No grant is acknowledged in the PubMed record.
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: see text] hr ⁻ ¹·nM ⁻ ¹) governing transitions between pro-inflammatory dominance and resolution phases. The model replicated experimentally observed cytokine dynamics, including TNF-α/IL-6 peaks (6-24 hours) and delayed IL-10 elevation (48 hours). Global sensitivity analysis highlighted IL-10 production ([Formula: see text]) and TNF-α suppression ([Formula: see text]) as key control parameters. Simulations predicted that IL-10 augmentation accelerates resolution, while TNF-α inhibition attenuates IL-10 induction, potentially compromising long-term recovery. By integrating dynamical systems theory with translational immunology, this model provides a mechanistic basis for optimizing immunomodulatory therapies in stroke and related inflammatory pathologies.
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