β‑glucan, a dectin‑1 ligand, promotes macrophage M1 polarization via NF‑κB/autophagy pathway.

β‑glucan, a dectin‑1 ligand, promotes macrophage M1 polarization via NF‑κB/autophagy pathway. Int J Oncol. 2018 Nov 09;: Authors: Li X, Luo H, Ye Y, Chen X, Zou Y, Duan J, Xiang D Abstract Pro‑inflammatory (M1) macrophages have key roles in atherogenesis. As β‑glucan has been demonstrated to exert pro‑inflammatory effects, the present study examined whether β‑glucan exerts atherogenic effects via converting macrophages into M1 phenotype. The results from reverse transcription‑quantitative polymerase chain reaction, flow cytometry, western blotting and transmission electron microscope indicated that M1 macrophage markers inducible nitric oxide synthase and cluster of differentiation 80 were upregulated, dectin‑1 (a receptor for β‑glucan) expression and nuclear factor (NF)‑κB nuclear translocation were promoted, and autophagy level was inhibited following β‑glucan treatment of macrophages. Additionally, dectin‑1 small interfering RNA (siRNA), autophagy inducer rapamycin and NF‑κB inhibitor SN50 reversed the effects of β‑glucan on autophagy level and macrophage M1 polarization, suggesting that dectin‑1 and NF‑κB are upstream of autophagy in β‑glucan‑induced macrophage M1 polarization. Notably, simultaneous treatment with dectin‑1 siRNA and SN50 exhibited similar effects on β‑glucan‑reduced autophagy compared with dectin‑1 siRNA treatment alone. These findings demonstrate that d...
Source: International Journal of Oncology - Category: Cancer & Oncology Authors: Tags: Int J Oncol Source Type: research