Takeshi Kusunoki, Noritsugu Ono and Katsuhisa Ikeda
Background: Chronic rhinosinusitis with eosinophilic infiltration (ECRS) has been noted a severe and intractable type of rhinosinusitis, which is often associated with asthma. Macrophages as well as eosinophilic infiltration have been reported to take part in the processes of severe asthma. Mucus hypersecretion and persistent airway inflammation results from the increased expression of mucin gene (MUC5AC). Oxidants are well known to induce the characteristic features that aggravate asthma. Superoxide dismutase (SOD), a cytoprotective enzyme against oxidants, has been extensively studied in airway diseases. From the viewpoint of “One way one disease”, we examined whether SOD could be associated with infiltrating macrophages, MUC5AC and other factors that exacerbate the rhinosinusitis.
Methods: Parts of each specimen derived from the nasal polyps of ECRS and chronic rhinosinusitis without eosinophilic infiltration (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 copper/zinc-superoxide dismutase (Cu, Zn-SOD) and macrophages by using CD68 and IL-17A as factors that promoteMUC5AC.
Results: The mean numbers of macrophages (CD68 positive cells) and IL-17A positive cells in the ECRS were significantly greater than in non-ECRS. The mean percentage of epithelial cells with Cu, Zn-SOD positive reaction in non-ECRS was significantly greater than in ECRS. There were significant negative correlations in all cases between Cu, Zn-SOD and CD 68, IL-17A or MUC5AC.
Conclusions: Our study suggests that loss of Cu, Zn-SOD in epithelia of ECRS could increase both IL-17 A and MUC5AC, resulting in the infiltration of macrophages and mucus over production.
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