Fig. 3
From: Functional integration of natural killer cells in a microfluidically perfused liver on-a-chip model
Stimulation with TLR-receptor agonists (LPS and Pam3CSK4) revealed a trend to higher expression of the maturation and cytotoxicity marker NKp46 on the endothelial layer of the liver-on-a-chip model (A). Increased TNF-alpha (B) and IL-6 (C) secretion of liver-on-a-chip including NK cells after 24 h perfusion with TLR-receptor agonists. Liver injury, reflected by endothelial cell layer disruption, assessed by immunofluorescence of VE-cadherin, was significantly increased after TLR-receptor agonist stimulation than in controls (D). Representative immunofluorescence image (E) showing disruption of the endothelial layer after application of the TLR receptor agonists. Figures A–D present data of at least three independent experiments, p-values are assessed by Mann Whitney test