Figure 11.

RBCm-cloaking NPs systems. (a) Fabricating illustration and model structure of RBCm-cloaking NPs: RBCm-cloaking Au NPs, DOX-loaded RBCm-cloaking PLA NPs, Van-loaded RBCm-cloaking gelatin NPs, RBCm-cloaking PLGA NPs, Targeting RBCm-cloaking PLGA NPs and toxin-detainment RBCm-cloaking PLGA NPs. (b) TEM image of folic acid modified RBCm-cloaking PLGA NPs (unpublished data). (c) Schematic structure of toxin nanosponges and their mechanism of neutralizing PFTs. The nanosponges consist of substrate-supported RBC bilayer membranes into which PFTs can incorporate. After being absorbed and arrested by the nanosponges, the PFTs are diverted away from their cellular targets, thereby avoiding target cells and preventing toxin-mediated haemolysis. (d) Survival rates of mice over a 15-day period following intravenous injections of 120 μg/kg Hla on day 21 via the tail vein (n=10). Unvaccinated mice were used as negative control and mice vaccinated with heat-treated Hla served as positive controls. Both the prime-only schedule and prime-boost schedule were conducted. (e) Comparison of skin lesion size following subcutaneous injections of 5 μg of Hla on day 21. Lesion size was measured for 14 days following the challenge (n=6). (Unvaccinated mice (black triangles, solid line) and mice vaccinated with heattreated Hla (prime; blue squares, dashed line), nanotoxoid(Hla) (prime; blue circles, solid line), heat-treated Hla (prime+boost; red squares, dashed line) or nanotoxoid(Hla) (prime+boost; red circle, solid line) received intravenous or subcutaneous administration of Hla.) Reproduced with permission³¹, ³². Copyright 2014, Nature.