[Effects on chemotactic factor expression in bronchial epithelial cells by co-stimulation of poly(I:C) and lipopolysaccharide and the underlying mechanism].

AIM: To investigate the effect of co-stimulation of mimic viral infection [polyinosinic: polycytidylic acid, poly(I:C)] and endotoxin (lipopolysaccharide, LPS) on chemotactic factors production of human bronchial epithelial cells and explore its related mechanism. METHODS: Human bronchial epithelial cells (16HBE) were challenged by co-stimulation of different concentrations of poly(I:C) and LPS. Some other 16HBE cells, before the co-stimulation of poly(I:C) and LPS, were pretreated with dexamethasone and p38MAPK specific inhibitor (SB203580), respectively. The levels of IL-8/CXCL8 and IP-10/CXCL1 mRNA transcription were detected by RT-PCR after 6 h challenge. The contents of IL-8 and IP-10 proteins were detected by ELISA after 24 h challenge. RESULTS: (1) The mRNA and protein expression of IL-8, not IP-10, increased under 10 µg/mL LPS stimulation compared with control group. The mRNA and protein expressions of both IL-8 and IP-10 were elevated significantly by the co-stimulation of LPS and 0.1 µg/mL poly (I:C) compared with control group and simple LPS groups. (2) The mRNA and protein expressions of IL-8 and IP-10 increased under the challenge of different concentrations of poly(I:C) (0.001, 0.01, 0.1 µg/mL) in a concentration-dependent manner, which showed no change after adding 10 µg/mL LPS. (3) Dexamethasone (1 µmol/L) and SB203580 (20 µmol/L) significantly decreased both the mRNA and protein production of IL-8 and IP-10 induced by co-stimulation of 0.1 µg/mL poly (I:C) and 10 µg/mL LPS compared with the control group and control+DMSO group respectively (P<0.01 and P<0.05). Inhibitive effect of dexamethasone was stronger than that of p38MAPK inhibitor. CONCLUSIONS: The co-stimulation of poly(I:C) and LPS can induce chemokine expression of airway epithelial cells. Poly(I:C) enhances the IL-8 expression induced by single LPS challenge, which suggests that viral infection could enhance the inflammation resulted from bacterial colonization in airway. Glucocorticoid has the greater effect on the inhibition of chemotactic factors production than p38MAPK inhibitor. These two drugs have a potential therapeutic effect on AECOPD caused by viral infection.