Switch Off "Parallel Circuit": Insight of New Strategy of Simultaneously Suppressing Canonical and Noncanonical Inflammation Activation in Endotoxemic Mice

Adv Biosyst. 2020 Jun;4(6):e2000037. doi: 10.1002/adbi.202000037. Epub 2020 May 18.

Abstract

Sepsis is a life-threatening inflammatory disease with a high mortality rate and huge implicative costs. Lipopolysaccharide (LPS) from gram-negative bacteria activates toll-like receptor 4 (TLR4) and may trigger septic shock. However, potent TLR4 inhibitors TAK-242 and Eritoran have been terminated in phase III clinical trials because of inadequate efficacy. Inspired by the recently discovered intracellular, noncanonical LPS receptors, it is considered that TLR4-mediated canonical and caspase-mediated noncanonical inflammation can be seen as a "parallel circuit" to induce sepsis and endotoxemia. Logically, it is proposed that the dual inhibition of caspase-4/5/11 and TLR4 can be a potential novel strategy to develop new therapeutics for sepsis. To verify the strategy, two potential compounds are found: Luteolin and Diacerein with substantial antiinflammatory activity in vitro and in vivo. The results show that the survival rate of endotoxemic mice treated by these compounds is increased remarkably. LPS-induced organ damage is also prevented. Moreover, these compounds result in physical and mental recovery for endotoxemic mice. Notably, Luteolin exhibits better antiinflammatory activity than TAK-242 at comparable TLR4-inhibitory levels. These findings indicate that simultaneous inhibition of TLR4 and caspase-4/5/11 can be an anticipative strategy defeating sepsis and endotoxemia, which can be translated into significant medical and economic benefits.

Keywords: TLR4; caspase-4/5/11; noncanonical inflammation; pyroptosis; sepsis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anthraquinones / pharmacology*
  • Anti-Inflammatory Agents / pharmacology*
  • Caspases / metabolism
  • Endotoxemia* / drug therapy
  • Endotoxemia* / metabolism
  • Endotoxemia* / pathology
  • Humans
  • Luteolin / pharmacology*
  • Male
  • Mice
  • RAW 264.7 Cells
  • Sulfonamides / pharmacology*
  • THP-1 Cells
  • Toll-Like Receptor 4* / antagonists & inhibitors
  • Toll-Like Receptor 4* / metabolism

Substances

  • Anthraquinones
  • Anti-Inflammatory Agents
  • Sulfonamides
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4
  • ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate
  • diacerein
  • Caspases
  • Luteolin