ArticleJournal of thrombosis and haemostasis : JTH2026
Shear cytokine crosstalk is a determinant of SARS-CoV-2-induced endothelial pathophysiology and thrombosis in human vessel chips.
Article in Journal of thrombosis and haemostasis : JTH, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundSARS-CoV-2 infection is associated with systemic vasculopathy and thromboinflammation. However, the interaction between shear-dependent endothelial function, inflammatory signaling, and thrombosis during viral exposure remains incompletely defined due to limitations of conventional in vitro and animal models.
objectivesTo determine how flow modulates endothelial structure, barrier integrity, inflammatory activation, and thrombogenic responses during exposure to SARS-CoV-2 spike protein or the complete virus, with or without interleukin-6 (IL-6).
methodsA human endothelialized vessel chip platform was used to independently control flow (10 dyne/cm
resultsUnder static conditions, spike exposure disrupted endothelial morphology, disorganized intercellular junctions, and increased permeability. Flow mitigated these changes, preserving junctional organization and reducing barrier disruption during viral exposure. IL-6 induced cytoskeletal remodeling and barrier dysfunction, consistent with inflammatory activation. When shear stress, IL-6, and spike exposure were combined, flow preserved junctional architecture and reduced morphological injury, although IL-6-associated cytoskeletal alterations persisted. Flow reduced viral replication, permeability, and thrombotic markers by 40% to 60% compared with static or inflammatory conditions, whereas IL-6 increased these measures. vesicular stomatitis virus-ΔG-Spike and authentic SARS-CoV-2 produced concordant phenotypes across junctional metrics, intercellular adhesion molecule 1 induction, and replication.
conclusionFlow partially preserves endothelial homeostasis during viral and inflammatory challenges, limiting structural injury, viral replication, and thromboinflammatory activation. These findings highlight the vessel chip as a rigorous platform for dissecting flow-dependent vascular pathology.
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