RNase L Is Involved in Liposaccharide-Induced Lung Inflammation

Viruses. 2020 Jan 7;12(1):73. doi: 10.3390/v12010073.


RNase L mediates interferon (IFN) function during viral infection and cell proliferation. Furthermore, the role of RNase L in the regulation of gene expression, cell apoptosis, autophagy, and innate immunity has been well established in the last decade. Tissue distribution reveals that RNase L is highly expressed in the lung and other organs. However, the physiological roles of RNase L in the lung are largely unknown. In this study, we found that polysaccharide (LPS)-induced acute lung injury (ALI) was remarkably intensified in mice deficient in RNase L compared to wild type mice under the same condition. Furthermore, we found that RNase L mediated the TLR4 signaling pathway, and regulated the expression of various pro- and anti-inflammatory genes in the lung tissue and blood. Most importantly, RNase L function in macrophages during LPS stimulation may be independent of the 2-5A system. These findings demonstrate a novel role of RNase L in the immune response via an atypical molecular mechanism.

Keywords: Acute lung injury; LPS; RNase L; TLR4.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Endoribonucleases / genetics
  • Endoribonucleases / metabolism*
  • Gene Knockout Techniques
  • Immunity, Innate / genetics*
  • Lipopolysaccharides / pharmacology
  • Lung / drug effects
  • Lung / pathology
  • Mice
  • Pneumonia / metabolism*
  • Signal Transduction / drug effects
  • Toll-Like Receptor 4 / drug effects
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 4 / metabolism*


  • Lipopolysaccharides
  • Toll-Like Receptor 4
  • Endoribonucleases
  • 2-5A-dependent ribonuclease