To investigate the effects of miR-155 on expression of IL-6, IL-10 and MIP-2 in alveolar macrophages from mice with acute pulmonary injury induced by sepsis.

The 15 male SD mice (6-8 weeks, 18-20 g) were randomly divided into 3 groups: control, sepsis and miR-155 antagomir group. The cecal ligation and perforation (CLP) were used to prepare the animal model of acute lung injury with sepsis. Six hours after the model was successfully set up, The pathological changes of left lower lobe were observed under light microscope after slicing and HE dyeing. The right lower pulmonary lobe was used to measure the dry and wet weight ratio. Plasma IL-6, IL-10 and MIP-2 were detected by ELISA.

The HE staining results showed that alveolar structure destruction, inflammatory cell infiltration, pulmonary interstitial thickening and bleeding were observed in the sepsis and miR-155 antagomir group. They also showed that the ratio of dry and wet weight was significantly lower in the sepsis group than that of the control and miR-155 antagomir group, and the difference was found to be statistically significant (P<0.05). The results of ELISA showed that the level of MIP-2, IL-6 in the plasma of septic group were significantly higher than those of the control and the miR-155 antagomir group, and the level of MIP-2 and IL-6 in the plasma of the miR-155 antagomir group were higher than those of the control group (P<0.05). The level of IL-10 in the plasma of the septic group was significantly lower than that of the control and the miR-155 antagomir group, and the level of IL-10 in the plasma of the miR-155 antagomir group was lower than that of the control group (P<0.05).

Overexpression of miR-155 in mice with acute lung injury induced by sepsis can promote the release of a large number of anti inflammatory factors, inhibit the expression of anti inflammatory factors in alveolar macrophages and lead to an imbalance between the pro-inflammatory and anti-inflammatory factors, resulting in an inflammatory reaction. However, miR-155 antagomir can inhibit the expression of miR-155, which can further inhibit the alveolar macrophages to release anti-inflammatory factors IL-6 and chemokine macrophage MIP-2, and raise the expression of anti-inflammatory factor IL-10 cells. It further prevents the accumulation of neutrophil and alveolar macrophages, effectively controls the occurrence of lung inflammation, and plays a protective role in lung.