Hypothermia alleviated LPS-induced acute lung injury in Rat models through TLR2/MyD88 pathway

Exp Lung Res. 2018 Oct-Nov;44(8-9):397-404. doi: 10.1080/01902148.2018.1557299. Epub 2019 Jan 19.

Abstract

Acute lung injury (ALI) is a common clinical syndrome in ICU departments with high mortality. The pathology of ALI is still not clear and there is no specific and efficient treatment against ALI. In this study, we established ALI rat model through lipopolysaccharide administration. We found that hypothermia therapy led to significant improvement in oxygenation index, edema formation and pathological score, demonstrating that hypothermia is beneficial to the recovery of lung function and alleviation of lung injury. Besides, hypothermia resulted in a decrease in plasminogen activator inhibitor-1(PAI-1) concentration, showing the inflammation was partially inhibited. This was also confirmed by a decrease in TNF-α mRNA and protein level in hypothermia group. The effect of hypothermia was mediated by TLR2/MyD88 signaling, which led to the alteration in NF-κB p65 level. Collectively, this study indicated that hypothermia therapy was potentially an efficient therapy against ALI.

Keywords: Acute lung injury; TLR2/MyD88 signaling; hypothermia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / chemically induced
  • Acute Lung Injury / therapy*
  • Animals
  • Hypothermia, Induced*
  • Lipopolysaccharides
  • Myeloid Differentiation Factor 88 / metabolism*
  • Rats
  • Signal Transduction
  • Toll-Like Receptor 2 / metabolism*

Substances

  • Lipopolysaccharides
  • Myeloid Differentiation Factor 88
  • Toll-Like Receptor 2