Interleukin-33 plays an important role in sepsis-induced acute lung injury in mice

Evidence has shown that Interleukin-33 (IL-33) plays a key role in the early induction and further amplification of sepsis. However, it remains unknown whether IL-33 has effects on sepsis-induced acute lung injury (ALI) and, if so, whether p38MAPK signaling pathway plays any role in it. This study was designed to insight the role of IL-33 in sepsis-induced ALI, and to discover the relationship between IL-33 and p38MAPK signaling pathway. Sepsis was induced in mice by intraperitoneal injecting LPS. The mice in the control group were intraperitoneal injected with normal saline, while the mice in sepsis groups were injected with 5 mg/kg LPS. For assessment of lung injury and biochemical studies, mice were weighed and sacrificed at different time points (6 h, 12 h, 24 h) after administration of LPS. Lung edema was assessed by determining the ratio of lung wet weight to total body weight. Serum levels of IL-6, TNF-α and IL-10 were measuredC. LPS-12 h group. D. LPS-24 h group by Elisa and the protein levels of IL-33, p38MAPK and p-p38MAPK were measured by Western blot analysis. The results showed that the expression level of IL-33 in sepsis groups was increased at the 6 h and 12 h, but decreased at the 12 h. The levels of IL-6 and TNF-α were correlated with the level of IL-33. What’s more, the protein level of IL-33 was related to the phosphorylation of p38MAPK. It indicates that IL-33 plays an important role in sepsis-induced ALI, which may be a new target for clinical intervention and treatment.