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Cyclic AMP signaling enhances lipopolysaccharide sensitivity and interleukin-33 production in RAW264.7 macrophages

Shizuka Sato1, Yoshiki Yanagawa1, Sachiko Hiraide1

  • 1Department of Pharmacology, School of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Kanazawa 1757, Ishikari-Tobetsu 061-0293, Japan.

Microbiology and Immunology
|April 10, 2016
PubMed

Insights

Cyclic adenosine monophosphate (cAMP) signaling enhances macrophage sensitivity to lipopolysaccharide (LPS), boosting Interleukin-33 (IL-33) production. This suggests stress-induced adrenaline may contribute to IL-33-related disorders.

Area of Science:

  • Immunology
  • Cellular Biology
  • Molecular Signaling

Background:

  • Interleukin-33 (IL-33) is implicated in various disorders, but its production stimuli are not well understood.
  • Macrophage activation by lipopolysaccharide (LPS) is a key immune response, with varying outcomes depending on LPS dose.
  • Cyclic adenosine monophosphate (cAMP) signaling pathways regulate numerous cellular functions, including immune responses.

Purpose of the Study:

  • To investigate the role of cAMP signaling in modulating IL-33 production by macrophages.
  • To determine how different doses of LPS affect IL-33 and TNF production in RAW264.7 macrophages.
  • To explore the involvement of protein kinase A (PKA) in cAMP-mediated IL-33 induction.

Main Methods:

  • RAW264.7 macrophages were treated with varying doses of LPS.
  • The effects of cAMP analogs (8-Br-cAMP) and cAMP-increasing agents (adrenaline) on IL-33 production were assessed.
  • mRNA levels and protein production of IL-33 and TNF were measured.
  • The impact of a PKA inhibitor (H89) on IL-33 induction was evaluated.

Main Results:

  • High-dose LPS induced both IL-33 and TNF production in macrophages.
  • Low-dose LPS induced TNF but not IL-33 production.
  • cAMP signaling (via 8-Br-cAMP or adrenaline) significantly enhanced low-dose LPS-induced IL-33 production at both mRNA and protein levels.
  • PKA inhibition blocked the enhancing effects of cAMP signaling on IL-33 production.

Conclusions:

  • cAMP-mediated signaling enhances the sensitivity of macrophages to LPS, specifically increasing IL-33 production.
  • Stress-induced factors like adrenaline may promote IL-33 production in macrophages.
  • This mechanism could link stress, macrophage activation, and the pathogenesis of IL-33-associated diseases.
Keywords:
cyclic AMPinterleukin-33lipopolysaccharidemacrophages

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