Additive Suppression of LPS-Induced IL-10 and TNF-alpha by Pre-treatment of Dexamethasone and SB203580 in a Murine Alveolar Macrophage Cell Line (MH-S)

作者：Meng, Aihong^*; Wang, Bin; Zhang, Xiaopeng; Qi, Na; Liu, Dengchang; Wu, Jiakai

来源：Inflammation, 2015, 38(3): 1260-1266.

DOI：10.1007/s10753-014-0093-x

• P38MAPK inhibitors
• glucocorticoids
• signal transducers and activators of transcription-3
• tumor necrosis factor-alpha
• interleukin-10

P38 inhibitors are potent anti-inflammatory agents with distinctive mechanism of action from corticosteroid; the potential combined use of both anti-inflammatory agents could be an effective treatment for inflammatory lung disease; however, the impact of such combination on the homeostasis of immune response was poorly understood. To investigate the combined effect of dexamethasone (DEX) and/or SB203580 on tumor necrosis factor (TNF)-alpha (pro-inflammatory) and interleukin (IL)-10 (anti-inflammatory) secretion in mouse alveolar macrophage cell line. Secreted TNF-alpha and IL-10 were measured by ELISA. Phosphorylated STAT3 were investigated using Western blotting and immunocytochemistry. Pre-treatment of DEX or SB203580 inhibited lipopolysaccharide (LPS)-stimulated IL-10, TNF-alpha secretion, and STAT3 phosphorylation. Combined use of both agents showed stronger inhibitory effect. Combining DEX and SB203580 showed strong inhibition on the LPS-induced IL-10 secretion and STAT3 phosphorylation, which might reflect a very important drawback from the combined use of both anti-inflammatory agents.

• 出版日期2015-6
• 单位河北省人民医院; 河北医科大学