Figure 1. . Inflammatory responses to chitosan depend on prior immune cell activation state, chitosan dose, and the presence of a tandem glucosamine motif.

In macrophages primed with phorbol ester (PMA), low doses of chitosan induce type 1 IFN, leading to increased IL-1ra and CXCL10/IP-10 release and low levels of IL-1β and PGE₂. High doses of chitosan activate the inflammasome, which leads to increased release of IL-1β and PGE₂, and suppressed release of IL-1ra and CXCL10/IP-10. When macrophages are polarized towards an M1 state, chitosan enhances the release of pro-inflammatory cytokines. In macrophages polarized towards an M2 state, chitosan enhances the release of anti-inflammatory cytokines.