Methods and Results: PS particles are taken up cellularly and increased the expression of inflammatory genes (e.g. Il-6 and Tnf-α) in all cell types, of oxidative stress-related genes (e.g. NADPH oxidase 1 and nitric oxide synthase 2) in monocytic and endothelial cells, and of the adhesion molecules Vcam-1 and Icam-1 in endothelial cells (3-6h, n=7-10). Investigating inflammatory cell adhesion, more adherent monocytic cells were detected on endothelial monolayer after PS particle stimulation under static as well as under flow conditions (n=6). Scratch assay revealed increased migration of monocytic cells after PS particle exposition, but regrowth of the artificial wound in epithelial cells and endothelial cells was attenuated (n=12-16). PS particles were able to pass a cell monolayer of epithelial cells in the transwell assay, demonstrating their ability to pass the epithelium (n=12-16) and furthermore led to increased epithelial permeability after exposure to PS particles.
In vivo, i.v. injected TRITC-conjugated PS particles were taken up by Ly6G-positive cells in the peripheral blood and accumulated in the liver, accompanied by a strong up-regulation of the acute phase proteins Saa1, Saa2 and Saa3. Moreover, PS particles given by gavage – which mimics their uptake by food intake – increased the expression of inflammatory genes in the aorta.

Conclusion: Our data show that microplastics are capable of inducing numerous inflammatory effects in vitro and in vivo and should therefore be considered as a novel environmental risk factor for epithelial and endothelial inflammation.