Forskolin attenuates the NLRP3 inflammasome activation and IL-1β secretion in human macrophages

Pediatr Res. 2019 Dec;86(6):692-698. doi: 10.1038/s41390-019-0418-4. Epub 2019 May 13.

Abstract

Background: The treatment of nucleotide-binding domain and leucine-rich repeat containing family, pyrin domain containing 3 (NLRP3) inflammasome-mediated pediatric inflammatory diseases is challenging. Here we studied whether cyclic adenosine monophosphate (cAMP) elevator forskolin could attenuate the nigericin-induced NLRP3-inflammasome activation and interleukin-1β (IL-1β) secretion in human macrophages.

Methods: The proteins and messenger RNA (mRNA) levels of inflammasome structural proteins and proinflammatory cytokines were measured in forskolin-stimulated nigericin-activated human THP-1 macrophages and primary macrophages.

Results: Activation of THP-1 macrophages with nigericin increased the mRNA expression of NLRP3, IL-1β, and caspase-1 (P < 0.01). Forskolin stimulation had no effect on the mRNA expression of NLRP3, caspase-1, or IL-1β in nigericin-activated cells (P > 0.05), while their protein levels were significantly decreased (P < 0.05). Forskolin-mediated increase in cytoplasmic cAMP in non-activated cells was attenuated in nigericin-activated macrophages (P < 0.05). Basal IL-1β secretion increased from 584 to 2696 pg/mL (P < 0.01) in nigericin-activated macrophages; forskolin dose-dependently reduced the nigericin-induced secretion of mature IL-1β (P < 0.01). Forskolin also inhibited the IL-1β secretion from activated human primary macrophages.

Conclusions: Forskolin inhibits the NLRP3 inflammasome activation and the secretion of mature IL-1β, in human macrophages. Forskolin and other cAMP elevator drugs could represent a novel approach for treatment of diseases associated with excessive inflammasome activation, like pediatric inflammatory diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Caspase 1 / genetics
  • Cell Line
  • Colforsin / administration & dosage
  • Colforsin / pharmacology*
  • Dose-Response Relationship, Drug
  • Humans
  • Inflammasomes / drug effects*
  • Inflammasomes / metabolism
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism*
  • Interleukin-4 / genetics
  • Macrophages / drug effects*
  • Macrophages / metabolism
  • NLR Family, Pyrin Domain-Containing 3 Protein / genetics
  • NLR Family, Pyrin Domain-Containing 3 Protein / metabolism*
  • Nigericin / pharmacology
  • RNA, Messenger / genetics
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • IL1B protein, human
  • IL4 protein, human
  • Inflammasomes
  • Interleukin-1beta
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • NLRP3 protein, human
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Colforsin
  • Interleukin-4
  • Caspase 1
  • Nigericin