IL-35 ameliorates lipopolysaccharide-induced endothelial dysfunction by inhibiting endothelial-to-mesenchymal transition

Sepsis is a systemic inflammatory response syndrome (SIRS) caused mainly by bacterial infection. The morbidity and mortality rates of sepsis are extremely high. About 18 million people worldwide suffer from severe sepsis each year, and about 14,000 people die from it every day. Previous studies have revealed that endothelial dysfunction plays a vital role in the pathological change of sepsis. Furthermore, endothelial-mesenchymal transition (EndMT, EndoMT) is capable of triggering endothelial dysfunction. And yet, it remains obscure whether interleukin-35 (IL -35) can alleviate endothelial dysfunction by attenuating LPS-induced EndMT. Here, through in vivo and in vitro experiments, we revealed that IL -35 has a previously unknown function to attenuate LPS-induced endothelial dysfunction by inhibiting LPS-induced EndMT. Mechanistically, IL -35 acts by regulating the NF kappa B signaling pathway.