Chronic granulomatous disease (CGD) is an inherited disorder of the immune system due to mutations in gp91phox gene which coding for NOX2 protein. Bacterial and fungal infections are most common infections in CGD patients. β-glucan (curdlan) is the main component of the cell wall of Candida albicans. At present, the molecular mechanism of dectin-1 in macrophage which involved in immune inflammation induced by curdlan is not very clear. In order to study the molecular mechanism, we estimated the level of ROS production by luminal and Ampled Red; estimated levels of IL-1β by ELISA; and estimated NF-κB signaling pathway by immunofluorescence assay. Our results showed that curdlan induced ROS production in macrophage in a dose-dependent way. Dectin-1 deficiency can partially reduce ROS generation and partially block the activation of NF-κB signaling pathway. NOX2 deficient mice displayed high level of IL-1β after curdlan injection and IL-1β level decreased in NOX2 KO mice when dectin-1 was knocked out. IL-1β level in Dectin-1 KO mice was as same as in WT mice while significantly different from Dectin-1/NOX2 KO mice. In summary, curdlan can activate NOX2 to generate ROS through recognition of foreign pathogens by receptor dectin-1 which existed in macrophage cell surface. Besides that, immune response induced by curdlan activated NF-κB signaling pathway and increased IL-1β level through dectin-1. Dectin-1 was involved in this process, but it was not the only pattern recognition receptor.