Fig. 1.

Model of CSP-induced NLRP3 inflammasome activation and cross-presentation: Ag together with CSP (via adsorption or encapsulation) was internalized by APCs. The protonation of the amino groups (“proton sponge effect”) leads to an extensive inflow of ions and water into the lysosome, which caused the osmotic swelling and deconstruction of the lysosome. The entrapped components (CSP and Ag) were released and finally presented onto MHC I, by cytoplasm degradation (with proteosome and ER involved); After the rupture, lysosome enzymes, cathepsin B, was also leaked into the cytoplasm, which induced the assembly and activation of NLRP3 complex. The capacity of TLR4 stimulation of CSP also played an important role in the intracellular synthesis of pro IL-1β and triggered the secretion of IL-1β and inflammatory responses, together with NLRP3 activation. (Ag: antigen; CSP: chitosan particle.)