• Yonghui Yu, Xiao Li, Shaofang Han, Jingjie Zhang, Jing Wang, and Jiake Chai.
• China-Canada Joint Lab of Food Nutrition and Health (Beijing), Key Laboratory of Special Food Supervision Technology for State Market Regulation, Beijing Advanced Innovation Center for Food Nutrition and Human Health, Beijing Technology and Business University, 11 Fucheng Road, Haidian District, Beijing, 100048, China.
• Eur J Trauma Emerg Surg. 2023 Apr 1; 49 (2): 103510451035-1045.

BackgroundThe miRNA profile is changed after burn or sepsis and is involved in regulating inflammatory reactions. However, the function and molecular mechanism of miRNAs in regulating burn sepsis-induced acute kidney injury (AKI) are still unclear.MethodsIn this study, animal and cell sepsis models were established after burned rats were injected with lipopolysaccharide (LPS) or NRK-52E cells treated with LPS, respectively. Cytokine expression, inflammatory cell infiltration, serum creatinine (Scr) and kidney injury molecule-1 (KIM-1) levels were analysed after the indicated treatments.ResultsBurn sepsis increased the expression of inflammatory factors (TNF-α and IL-1β) and chemokines (MIP-1α, MIP-2 and MCP-1). Moreover, burn sepsis promoted macrophage and neutrophil infiltration into the kidney and upregulated the levels of Scr and KIM-1 in the kidney and urine. Ectopic expression of miR-181c significantly reduced LPS-induced TLR4 protein expression, suppressed KIM-1 mRNA levels and subsequently inhibited the activation of inflammatory genes (TNF-α and IL-1β) and chemokine genes (MIP-1α, MIP-2 and MCP-1).ConclusionsOur results demonstrated that miR-181c could suppress TLR4 expression, reduce inflammatory factor and chemokine secretion, mitigate inflammatory cell infiltration into the kidney and downregulate KIM-1 expression, which might ultimately attenuate burn sepsis-induced AKI.© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.

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