To investigate the impact of the stimulator of interferon genes (STING) on the repair process of acute lung injury in mice and its influence on macrophages efferocytosis.

Twenty-five C57BL/6 mice aged 10-12 weeks were randomly divided into a D0 group, a D1 group, a D3 group, a D5 group and a D7 group, with five mice in each group, and the mice samples were collected after 0, 1, 3, 5 and 7 days of an intratracheal injection of 0.5 mg/kg lipopolysaccharide (LPS) respectively. In addition, five STING wild-type (STING^+/+) mice and five STING knockout (STING^-/-) mice were selected and divided into a STING^+/+ + LPS group and a STING^-/- + LPS group, and the mice samples were collected after 5 days of an intratracheal injection of 0.5 mg/kg LPS. Hematoxylin eosin (HE) staining was employed to observe the pathological changes in lung tissue, and the cell count, neutrophil count and protein concentration in alveolar lavage fluid were detected to access the degree of lung injury. Apoptotic neutrophils were injected into the trachea of mice, and alveolar lavage fluid cells were collected 3 hours later for flow cytometry to determine the efferocytosis rate of macrophages. TUNEL and F4/80 double staining of lung tissues were conducted via immunofluorescence to evaluate efferocytosis. The phenomenon of macrophage efferocytosis was observed through Pap staining.

The C57BL/6 mice reached the peak of lung injury 3 days after induction of acute lung injury and began to repair after 5 days, and in the absence of treatment, the repair was basically completed within 7 days. After 5 days of acute lung injury, the lung tissue injury score and the protein concentration, total cell count and neutrophil count in alveolar lavage fluid of mice in the STING^-/- + LPS group were lower than those in the STING^+/+ + LPS group (t = 3.257, 2.926, 3.946, 2.669; P = 0.012, 0.019, 0.004, 0.028). Flow cytometry and immunofluorescence staining showed that the efferocytosis rates of alveolar macrophages in the STING^-/- + LPS group were significantly higher than those in the STING^+/+ + LPS group (t = 3.143, 6.963; P = 0.016, < 0.001).

Deletion of STING may regulate the repair process of acute lung injury through enhancing macrophage efferocytosis. Therefore, this study provides new insights into the role of STING in the lung injury and repair.