BACKGROUND AND OBJECTIVE: CD163 is a monocyte/macrophage-specific molecule whose expression is induced by corticosteroids and IL-10. The aim of this study was to evaluate the concentration of soluble CD163 (sCD163) in the induced sputum of asthmatic patients before and after therapy with inhaled corticosteroids (ICSs). PATIENTS AND METHODS: The study was performed in 24 patients with mild allergic asthma (AAs) and 10 healthy controls (HCs). In 18 AAs, induced sputum and serum samples were obtained before ICS therapy (T0) and 7 days later (T7). In the 6 AAs not treated with ICSs the procedures were performed at To and T7. The concentration of sCD163 in sputum and serum samples was evaluated using ELISA. RESULTS: There was no significant difference in mean (SD) baseline serum sCD163 concentration between AAs (1030 [449] ng/mL) and HCs (930 [334.5] ng/mL, P = .530). However, at To the mean sputum sCD163 concentration was significantly greater in AAs (4.78 [3.34] ng/mL) than in HCs (1.8 [0.41] ng/mL, P =.009). Treatment with ICSs resulted in a significant increase in sCD163 concentration in sputum (P < .0001) but not in serum (P =.679). No change in sputum or serum sCD163 concentration was detected in AAs who were not treated with ICSs. The change in sputum sCD163 concentration inversely correlated with changes in sputum eosinophilia or exhaled nitric oxide concentration. CONCLUSIONS: ICS therapy leads to local upregulation of sCD163 expression, which in turn may participate in the anti-inflammatory effects of ICS therapy.
BACKGROUND AND OBJECTIVE:CD163 is a monocyte/macrophage-specific molecule whose expression is induced by corticosteroids and IL-10. The aim of this study was to evaluate the concentration of soluble CD163 (sCD163) in the induced sputum of asthmatic patients before and after therapy with inhaled corticosteroids (ICSs). PATIENTS AND METHODS: The study was performed in 24 patients with mild allergic asthma (AAs) and 10 healthy controls (HCs). In 18 AAs, induced sputum and serum samples were obtained before ICS therapy (T0) and 7 days later (T7). In the 6 AAs not treated with ICSs the procedures were performed at To and T7. The concentration of sCD163 in sputum and serum samples was evaluated using ELISA. RESULTS: There was no significant difference in mean (SD) baseline serum sCD163 concentration between AAs (1030 [449] ng/mL) and HCs (930 [334.5] ng/mL, P = .530). However, at To the mean sputum sCD163 concentration was significantly greater in AAs (4.78 [3.34] ng/mL) than in HCs (1.8 [0.41] ng/mL, P =.009). Treatment with ICSs resulted in a significant increase in sCD163 concentration in sputum (P < .0001) but not in serum (P =.679). No change in sputum or serum sCD163 concentration was detected in AAs who were not treated with ICSs. The change in sputum sCD163 concentration inversely correlated with changes in sputum eosinophilia or exhaled nitric oxide concentration. CONCLUSIONS: ICS therapy leads to local upregulation of sCD163 expression, which in turn may participate in the anti-inflammatory effects of ICS therapy.