172 Correlation between CU/ZN-SOD and Macrophages or MUC5AC in Eosinophilic Chronic Rhinosinusitis With Nasal Polyps

BACKGROUND: Recently, some researchers have reported that increases and decreases of infiltrating macrophages, a mucin gene or the antioxidant as well as infiltrating eosinoplils would be related to severe asthma. At present, eosinophilic chronic rhinosinusitis with nasal polyps (ECRS) has been considered intractable rhinosinusitis. From the point view of “one air way, one disease,” we immunologically examined macrophages and mucin gene(MUC5AC), IL-17A with these promotive factors and Copper-and Zinc-containing superoxide dismutase (Cu/Zn-SOD). Furthermore, we discuss whether Cu/Zn-SOD would be associated with infiltrating macrophages, MUC5AC and IL-17A. METHODS: The patients were classified into ECRS and non-eosinophilic chronic rhinosinusitis with nasal polyps (non-ECRS) groups. In addition, normal mucosal membranes of the sphenoid sinus removed at operation for pituitary adenoma were used as control. Part of each specimen derived from the nasal polyps of ECRS and non-ECRS were divided and fixed in 10% phosphate buffered formalin, embedded in paraffin, processed routinely and then prepared as semi-thin sections (3.5 μm). We immunohistochemically observed Cu/Zn-SOD and macrophages by using CD68, IL-17A, and MUC5AC. RESULTS: Both the numbers of macrophages (CD 68 positive cells) and IL-17A-positive cells in the ECRS were significantly greater than in non-ECRS. Furthermore, there was a significant correlation between CD 68 and IL-17A positive cells. The rate of epithelial cells with MUC5AC-positive reaction was significant in the comparison of ECRS with non-ECRS. On contrast, the rate of Cu/Zn-SOD-positive epithelial cells in non-ECRS was significantly greater than that in ECRS. Cu/Zn-SOD was inversely and significantly correlated with macrophages, IL-17A, and MUC5AC. CONCLUSIONS: The present study suggested that the decrease of Cu/Zn-SOD in ECRS could be increased by the infiltration of macrophages, the expression of IL-17A, and MUC5AC.