Charge-biased nanofibrous membranes with uniform charge distribution and hemocompatibility for enhanced selective adsorption of endotoxin from plasma

Endotoxin has been recognized as the crucial inducer for sepsis, and selective removal of endotoxin from plasma in vitro is the popular therapeutic strategy, such as hemoperfusion technology based on adsorption. Construction of hemoperfusion adsorbents with high endotoxin adsorption capacity in plasma is critical to meet the demands of hemoperfusion therapy for sepsis. However, it has proven to be challenging because of the adhesion of plasma protein. Inspired by the antiadhesion property of mixed-charge polymers and the endotoxin adsorption property of polyethyleneimine, here, a charge-bias, endotoxin selectively adsorbable and hemocompatible layer was constructed on nanofibrous surface of polysulfone (PSF) electrospun nanofibrous membrane (ENM) by the co-deposition of positively-charged polyethyleneimine (PEI) and negatively-charged polydopamine (PDA). The charge-bias degree of PEI/PDA co-deposition layer was quantified through zeta potential measurement, and firstly visualized through Kelvin probe force microscopy (KPFM) measurement. The continuity and integrity of PEI/PDA layer were characterized by XPS and TEM. We showed that the light positive charge-bias of the PEI/PDA layer in physiological environment (pH = 7.4) can macroscopically drove the adsorption selectivity towards endotoxins via electrostatic interaction, and uniformly distributed positive and negative charges can microscopically drove the anti-protein adhesion property. The resultant PEI/PDA@PSF ENM exhibited high adsorption capacity of 9049 EU/g in plasma, which is much higher than commercial endotoxin adsorbents. Notably, PEI/PDA@PSF ENM possessed satisfactory anti-plasma protein adhesion property, hemocompatibility and had no adverse effects on blood components, especially plasma protein. This work suggests a feasible approach for producing ENMs-based hemoperfusion adsorbent matrix for endotoxin-induced sepsis.