Inflammatory cell infiltration contributes to the pathogenesis of acute respiratory distress syndrome (ARDS). Protectin DX (PDX), an endogenous lipid mediator, shows anti‐inflammatory and proresolution bioactions. In vivo, the mice were intraperitoneally injected with PDX (0.1 µg/mouse) after intratracheal (1 mg/kg) or intraperitoneal (10 mg/kg) LPS administration. Flow cytometry was used to measure inflammatory cell numbers. Clodronate liposomes were used to deplete resident macrophages. RT‐PCR, and ELISA was used to measure MIP‐2, MCP‐1, TNF‐α and MMP9 levels. In vitro, sorted neutrophils, resident and recruited macrophages (1 × 10⁶) were cultured with 1 μg/mL LPS and/or 100 nmol/L PDX to assess the chemokine receptor expression. PDX attenuated LPS‐induced lung injury via inhibiting recruited macrophage and neutrophil recruitment through repressing resident macrophage MCP‐1, MIP‐2 expression and release, respectively. Finally, PDX inhibition of neutrophil infiltration and transmembrane was associated with TNF‐α/MIP‐2/MMP9 signalling pathway. These data suggest that PDX attenuates LPS‐stimulated lung injury via reduction of the inflammatory cell recruitment mediated via resident macrophages.

中文翻译：

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PDX通过LPS诱导的肺损伤中的驻留巨噬细胞调节炎性细胞浸润。

炎性细胞浸润促成急性呼吸窘迫综合征（ARDS）的发病机理。Protectin DX（PDX）是一种内源性脂质介体，具有抗炎和促分辨率的生物作用。在体内，在气管内（1 mg / kg）或腹膜内（10 mg / kg）LPS给药后，给小鼠腹膜内注射PDX（0.1 µg /小鼠）。流式细胞仪用于测量炎症细胞数量。氯膦酸盐脂质体用于消耗常驻巨噬细胞。RT-PCR和ELISA用于测量MIP-2，MCP-1，TNF-α和MMP9水平。体外，分选的嗜中性粒细胞，常驻和募集巨噬细胞（1×10 ⁶）用1μg/ mL LPS和/或100 nmol / L PDX培养以评估趋化因子受体的表达。PDX通过分别抑制常驻巨噬细胞MCP-1，MIP-2的表达和释放，通过抑制募集的巨噬细胞和嗜中性白细胞的募集来减轻LPS诱导的肺损伤。最后，PDX抑制中性粒细胞浸润和跨膜与TNF-α/ MIP-2 / MMP9信号通路相关。这些数据表明PDX通过减少由驻留巨噬细胞介导的炎症细胞募集而减轻了LPS刺激的肺损伤。