Ligand Binding to the (1→3)-β-D-Glucan Receptor Stimulates Nfκb Activation, but Not Apoptosis in U937 Cells

Recent data suggest that sepsis stimulates macrophage apoptosis (A(o)) with subsequent induction of macrophage dysfunction. Nuclear factor-kappaB (NFκB) activation has been linked to A(o) in either a pro- or antiapoptotic role. Glucans are biological response modifiers which exert antisepsis activity. This investigation examined the effect of (1-3)-β-D-glucan receptor binding by a high affinity ligand on A(o) and NFκB activation in U937 cells in the presence or absence of LPS. A high affinity glucan ligand (IC50 = 23 nM) activated NFκB, but did not induce A(o) or significantly alter LPS induced U937 A(o). These data indicate that: i) modulation of the macrophage (1-3)-β-D-glucan receptor stimulates NFκB; ii) does not induce A(o) or significantly diminish LPS induced A(o) and iii) activation of the U937 FAS receptor does not alter the relative A(o) responses in glucan and LPS treated cells