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Modulation of inflammation is a crucial component of the development of acute lung injury. A20, a ubiquitin editing enzyme, may regulate cellular inflammatory reactions, particularly those involving the signaling pathway of nuclear factor NF-κB (NF‑κB). The present study investigated the mechanism by which A20 downregulated NF‑κB and further contributed to macrophage polarization from the M1 to M2 phenotypes in lipopolysaccharide (LPS)‑induced lung injury. Sprague‑Dawley rats injected with LPS were used in the present study. Bronchoalveolar lavage fluid and lung tissue were collected from each experimental rat. A macrophage cell line was used to test the expression levels of A20. Tumor necrosis factor‑α (TNF‑α), interleukin‑1 beta (IL‑1β) and NF‑κB activities were assessed by ELISA and polymerase chain reaction. Macrophage phenotypes were assayed using fluorescence‑activated cell sorting. Elevated levels of TNF‑α, IL‑1β, NF‑κB and A20 were observed in the macrophages of rats treated with LPS. Furthermore, A20 overexpression inhibited NF‑κB DNA binding activity and increased macrophage polarization from the M1 to M2 phenotype in lung macrophages of the NR8383 cell line. It was concluded that the A20 protein in macrophages modulates lung injury induced by LPS. The overexpression of A20 in macrophages may be involved in modulating macrophage polarization. The mechanisms and molecular identification of macrophage polarization activation may provide a basis for the treatment of inflammation in lung injury.

A20 protein regulates lipopolysaccharide-induced acute lung injury by downregulation of NF-κB and macrophage polarization in rats