Figure 2. Characterization and pathogen-binding efficiency of MNVs. a) Quantitative measurement of the pathogen-binding-related surface receptors on hRBC-MNVs and hWBC-MNVs (n = 3). b) Binding efficiencies of hRBC-MNVs, GYPA-blocked hRBC-MNVs, CR1-blocked hRBC-MNVs, GYPA-and CR1-blocked hRBC-MNVs to methicillin-resistant S. aureus (MRSA), extended-spectrum β-lactamase-positive E. coli (ESBL-EC), RSV, CMV, Zika virus (ZIKV) E protein, HCoV-OC43, and SARS-CoV-2 S protein in human plasma (n = 3). c) Binding efficiencies of hWBC-MNVs, CR1-blocked hWBC-MNVs, CR3-blocked hWBC-MNVs, and CR1-and CR3-blocked hWBC-MNVs to MRSA, ESBL-EC, RSV, CMV, ZIKV E protein, HCoV-OC43, and SARS-CoV-2 S protein in human plasma. d,e) Binding efficiencies of d) hRBC-MNVs and e) hWBC-MNVs to MRSA and ESBL-EC when supplemented with MBL, ficolin (FCN)-1, or C3b in TBS buffer (n = 3). f,g) Binding efficiencies of f) hRBC-MNVs and g) hWBC-MNVs to MRSA and ESBL-EC when supplemented with MBL, FCN-1, or C3b in human blood (n = 3). h,i) Binding efficiency of h) hRBC-MNVs and i) hWBC-MNVs to HCoV-OC43, RSV, CMV, SARS-CoV-2 S protein, and Zika virus (ZIKV) E protein in TBS buffer supplemented with MBL, FCN-1, or C3b. j) Binding efficiency of hWBC-MNVs to SARS-CoV-2 S protein when supplemented with MBL, FCN-1, or anti-SARS-CoV-2 S protein immunoglobulin G (IgG) (n = 3). k) D-glucose depletion in diabetic rat blood by repetitive incubation and magnetic depletion using hRBC-MNVs. l) MRSA spiked in diabetic rat blood was magnetically depleted using hRBC-MNVs. m) Fecal bacterial concentrations in human whole blood were significantly (99.97%) reduced after a single round of magnetic depletion using hRBC-MNVs (n = 3). n) The removal efficiency of SARS-CoV-2 spike protein and their variants (B.1.1.7, B.1351, B.1.617.2 and B.1.1.529) using hWBC-MNVs (n = 3). Data were expressed as means ± SEM. Statistical significance was calculated by a two-tailed Student's t test. *P < 0.05; **P < 0.005; ***P < 0.001; NS, not significant.

Autologous implantable scaffolds that induce vasculogenesis have shown great potential in tissue regeneration; however, previous attempts mainly relied on cell-laden hydrogel patches using fat tissues or platelet-rich plasma, which are insufficient for generating a uniform vasculature in a scalable manner. Here, implantable vascularized engineered thrombi (IVETs) are presented using autologous whole blood, which potentiate effective skin wound healing by constructing robust microcapillary vessel networks at the wound site. Microfluidic shear stresses enable the alignment of bundled fibrin fibers along the direction of the blood flow streamlines and the activation of platelets, both of which offer moderate stiffness of the microenvironment optimal for facilitating endothelial cell maturation and vascularization. Rodent dorsal skin wounds patched with IVET present superior wound closure rates (96.08 ± 1.58%), epidermis thickness, collagen deposition, hair follicle numbers, and neutrophil infiltration, which are permitted by enhanced microvascular circulation. Moreover, IVET treatment accelerates wound healing by recruiting M2 phenotype macrophages.