NLRC5 negatively regulates inflammatory responses in LPS-induced acute lung injury through NF-κB and p38 MAPK signal pathways

Acute lung injury is an acute inflammatory disease with high morbidity rate and high mortality rate. However, there is still no effective clinical treatment to date. Our previous studies found that NLRC5 was significantly increased in acute liver injury model induced by LPS to reduce the secretion of IL-6 and TNF-alpha. Nevertheless, there is no report on the role of NLRC5 in regulating the development of acute lung injury. In this study we successfully established a model of acute lung injury induced by tracheal instillation of LPS in mice, and found NLRC5 expression was apparently elevated in mouse lung tissue and primary alveolar macrophages. NLRC5 overexpression negatively regulated secretion of inflammatory cytokines in murine alveolar macrophage cells through NF-kappa B and p38 MAPK pathway inhibition. There is a positively feedback between NLRC5 and NF-kappa B or p38 MAPK pathway. This study may provide some new ideas for clinical prevention of lung injury.