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Intraperitoneal injection of β-1,3-D-glucan coupled to the surface of monodisperse methacrylate microbeads improves the resistence against bacterial infections in mice, while methacrylate microbeads alone do not. The effect of the glucan-derivatized microbeads (GDM) is considered lo be mediated through peritoneal macrophages [34, 40].

We show that both GDM and (he underivatized methacrylate microbeads (UDM) treated with normal serum were rapidly bound and phagocytozed by mouse peritoneal macrophages in vitro. We found that both complement and fibronectin opsonized the bead.-; and were responsible for the uptake.

Treatment of microbeads with serum lacking fibronectin and complement activity still gave BOOK uptake of GDM, but not uptake of UDM. The uptake of GDM was similar to the uptake of untreated GDM and was inhibited by pretreatment of macrophages with soluble β-1,3-D-gluean.

Our conclusion is that GDM and UDM intraperitoneally bind fibronectin and C3 through activation of the alternative pathway of complement. This leads to their phagocytosis by macrophages through fibronectin and complement receptors. GDM are also internalized via β-glucan receptors. We present the hypothesis that the β-glucan receptors on peritoneal macrophages account for the protective effect of GDM in intraperitoneal bacterial infections.