探讨微小核糖核酸155（miR-155）对脓毒症急性肺损伤（ALI）肺泡巨噬细胞白介素（IL）-6、IL-10及巨噬细胞炎性蛋白2（MIP-2）的影响。

健康清洁C57BL/6雄性小鼠（6~8周，18~20 g）15只，随机分为对照组、脓毒症组和miR-155 antagomir 3组，每组5只，其中miR-155 antagomir组小鼠中将miR-155 antagomir试剂经尾静脉注射，对照组和脓毒症组小鼠注射等量0.9%NaCl，观察24 h后，脓毒症组和miR-155 antagomir组采用盲肠结扎穿孔（CLP）法制备脓毒症ALI动物模型，对照组仅翻动盲肠进行对照，观察3组小鼠生命体征变化，模型制备6 h后，3组小鼠均取左肺下叶行苏木精-伊红（HE）方法进行染色，在光镜下观察肺病理形态变化，取右肺下叶检测干湿重比，应用酶联免疫吸附试验（ELISA）检测血浆IL-6、IL-10、MIP-2浓度。

HE染色结果表明：脓毒症组和miR-155 antagomir组小鼠肺内均出现肺泡结构破坏、炎症细胞浸润、间质增厚、出血，miR-155 antagomir组肺组织炎性表现较脓毒症组显著减轻。3组干湿重比结果显示：脓毒症组干湿重比［（0.16±0.01）%］明显低于对照组［（0.22±0.01）%］和miR-155 antagomir组［（0.19±0.01）%］，miR-155 antagomir组低于对照组，差异具有统计学意义（均P<0.05）。ELISA结果显示：脓毒症组的血浆IL-6浓度［（171.35±10.41）pg/ml］、MIP-2浓度［（299.71±19.82）pg/ml］显著高于对照组［（125.74±4.41）pg/ml；（214.00±14.93）pg/ml］和miR-155 antagomir组［（144.41±6.29）pg/ml；（270.38±11.96）pg/ml］，IL-10浓度［（283.58±19.90 ）pg/ml］显著低于对照组［（370.27±15.41）pg/ml］和miR-155 antagomir组［（333.30±16.49）pg/ml］，miR-155 antagomir组的血浆IL-6、MIP-2浓度高于对照组，IL-10浓度明显低于对照组，差异具有统计学意义（均P<0.05）。

脓毒症ALI时miR-155过度表达，过度表达的miR-155能促进肺泡巨噬细胞释放大量促炎因子而抑制抗炎因子的表达，引起促炎因子及抗炎因子失衡，发生不可控炎症反应，而miR-155 antagomir能够拮抗miR-155的表达，抑制肺泡巨噬细胞释放促炎因子IL-6及趋化因子MIP-2，上调抗炎因子IL-10的表达，进一步抑制中性粒细胞及肺泡巨噬细胞聚集，防止产生更多的炎症介质，有效控制肺部炎症反应的发生，对肺起到一定的保护作用。

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.