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 (Ao) with subsequent induction of macrophage dysfunction. Nuclear factor-kappaB (NFκB) activation has been linked to Aoin 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 Aoand 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 Aoor significantly alter LPS induced U937 Ao. These data indicate that: i) modulation of the macrophage (1-3)-β-D-glucan receptor stimulates NFκB; ii) does not induce Aoor significantly diminish LPS induced Aoand iii) activation of the U937 FAS receptor does not alter the relative Aoresponses in glucan and LPS treated cells.