HSPA12B attenuates acute lung injury during endotoxemia in mice.

Acute lung injury (ALI) is a critical manifestation of sepsis/septic shock. Heat shock protein A12B an endothelial cell-expressed heat shock protein, shows a negative regulation of lipopolysaccharide (LPS)-induced inflammation in myocardium and endothelial cells. However, it is unclear whether exerts protective effects against ALI during sepsis/septic shock. In this study, we treated Hduanyu184212B transgenic mice (Tg) and wild type littermates (WT) with LPS for 6h to induce endotoxemia. LPS treatment significantly caused pulmonary injuries as evidenced by microarchitecture destruction, vascular leakage and neutrophil recruitment in lungs of WT mice. However, the LPS-induced pulmonary injuries were significantly attenuated in Tg mice. Moreover, the LPS-induced activation of extracellular signal-regulated kinases (ERKs) and upregulation of intercellular adhesion molecule-1 (ICAM-1) and Cyclooxygenase-2 (Cox-2) were inhibited in Tg lungs compared with that in WT mice. Additionally, Tg lungs showed a significant lower level of vascular endothelial growth factor (VEGF) compared with WT mice. Our results demonstrate a pulmonary protective effect of Hduanyu184212B against endotoxin challenge, which indicates management of Hduanyu184212B expression could serve as a potential therapeutic target for ALI during sepsis/septic shock.

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