Microplastic particles induce endothelial activation

Abstract

Background and Aims : Although microplastics being omnipresent in our environment and already detected in various organisms, less is known about the effects of microplastics on vascular biology in particular. Here we investigated the effects of carboxylated polystyrene (PS) microplastic particles (1 μm) on murine endothelial and immune cells, which are both crucially involved in vascular inflammation.Methods: Murine monocytic J774A.1 cells and endothelial MyEND cells were stimulated with PS particles (3/6 hrs, n=7-10). mRNA and protein levels were analyzed using real-time PCR and ELISA. Adhesion assays were performed incubating confluent MyEND cells with PS particles and Calcein-AM labelled J774A.1 (static/flow). Adherent J774A.1 were detected by fluorescence microscopy (n=6). C57BL/6J mice were injected with TRITC-conjugated PS i.v. (n=6/group). PS particles were localized in blood and liver using IHC staining.Results: In J774A.1 cells, PS particles induced Il1-β and Tnf-α expression and TNF-α release. In MyEND cells, PS particles up-regulated Icam-1 and Vcam-1 levels and sVCAM-1 release. PS particles induced adhesion of J774A.1 cells on endothelial monolayers under static as well as under flow conditions. In vivo, PS particles taken up by neutrophiles (Ly6G-positive) in the peripheral blood. PS particles accumulated in the liver, accompanied by a strong up-regulation of the acute phase proteins Saa1, Saa2 and Saa3. Moreover, Aortic tissue from mice injected with PS particles showed enhanced Il-1β and Vcam-1 expression.Conclusions: PS particles are able to activate the endothelium with subsequent monocyte adhesion, representing a hallmark of vascular inflammation. Thus, microplastics need to be evaluated as a potential novel environmental risk factor for endothelial inflammation. Background and Aims : Although microplastics being omnipresent in our environment and already detected in various organisms, less is known about the effects of microplastics on vascular biology in particular. Here we investigated the effects of carboxylated polystyrene (PS) microplastic particles (1 μm) on murine endothelial and immune cells, which are both crucially involved in vascular inflammation. Methods: Murine monocytic J774A.1 cells and endothelial MyEND cells were stimulated with PS particles (3/6 hrs, n=7-10). mRNA and protein levels were analyzed using real-time PCR and ELISA. Adhesion assays were performed incubating confluent MyEND cells with PS particles and Calcein-AM labelled J774A.1 (static/flow). Adherent J774A.1 were detected by fluorescence microscopy (n=6). C57BL/6J mice were injected with TRITC-conjugated PS i.v. (n=6/group). PS particles were localized in blood and liver using IHC staining. Results: In J774A.1 cells, PS particles induced Il1-β and Tnf-α expression and TNF-α release. In MyEND cells, PS particles up-regulated Icam-1 and Vcam-1 levels and sVCAM-1 release. PS particles induced adhesion of J774A.1 cells on endothelial monolayers under static as well as under flow conditions. In vivo, PS particles taken up by neutrophiles (Ly6G-positive) in the peripheral blood. PS particles accumulated in the liver, accompanied by a strong up-regulation of the acute phase proteins Saa1, Saa2 and Saa3. Moreover, Aortic tissue from mice injected with PS particles showed enhanced Il-1β and Vcam-1 expression. Conclusions: PS particles are able to activate the endothelium with subsequent monocyte adhesion, representing a hallmark of vascular inflammation. Thus, microplastics need to be evaluated as a potential novel environmental risk factor for endothelial inflammation.