In situ self-growth nano-selenium hydrogel coating alleviates surface thrombosis of blood-contacting devices by inactivating inflammatory cells.

The formation of thrombi in blood-contacting devices is accompanied by a several risks that can be life-threatening. Specifically, the process of blood exposure immediately after implantation triggers an immune response aimed at removing foreign substances, which can lead to thrombosis, inflammation and device malfunction. To confer anticoagulant properties to the implanted devices, a nano-selenium hydrogel coating which was in-situ self-growing on implant devices had been developed that inhibited thrombosis by intervening in the inflammatory cell activation pathway, possibly by decreasing tissue factor activity and thrombin production expressed by inflammatory cells. Compared with the selenium-free coating, the nano-selenium hydrogel coating significantly inhibited macrophage activation, as demonstrated by reduced M1 phenotype and increased M2 phenotype polarization, resulting in a 146 % increase in the M2/M1 ratio, together with the reduction of secretion of pro-inflammatory cytokines. More importantly, the selenium coating reduced macrophage procoagulant activity through macrophage inactivation, resulting in decreased tissue factor (TF) release and thrombin production. Remarkably, the coating suppressed the coagulation response in a rabbit model of LPS-induced inflammation and in patients with clinical sepsis, thereby reducing thrombus formation manifested by decreased fibrin deposition and reduced monocyte markers. Further studies demonstrated that coated central venous catheters (CVCs) in rabbit and pig vascular models diminished thrombosis and vascular inflammatory activation. Overall, this active anti-inflammatory hydrogel coating strategy is effective in inhibiting thrombus formation on blood-contacting device surfaces, especially in more challenging bloodstream environments.