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Mast cell tryptase induces microglia activation via protease-activated receptor 2 signaling

Shu Zhang1, Xiaoning Zeng, Haiwei Yang

  • 1Clinical Research Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|May 23, 2012
PubMed
Abstract

Insights

Mast cell tryptase activates brain microglia, releasing inflammatory factors via the PAR-2-MAPK-NF-kappa B pathway. This finding sheds light on microglia-mediated brain inflammation.

Area of Science:

  • Neuroimmunology
  • Cellular and Molecular Neuroscience

Background:

  • Mast cell tryptase is known to activate peripheral immune cells, contributing to inflammation.
  • The role of tryptase in activating microglia, the brain's resident immune cells, was previously uninvestigated.
  • Microglia are crucial for central nervous system (CNS) immune surveillance.

Purpose of the Study:

  • To investigate the effect of mast cell tryptase on microglia activation.
  • To elucidate the signaling pathways involved in tryptase-induced microglia activation.

Main Methods:

  • Primary microglia cultures were used to examine tryptase-induced activation.
  • Pro-inflammatory factors (TNF-alpha, IL-6), reactive oxygen species (ROS), and mitochondrial membrane potential were measured.
  • MAPK and NF-kappa B phosphorylation were assessed via Western blot.

Main Results:

  • Tryptase stimulated microglia activation, leading to the release of TNF-alpha, IL-6, and ROS.
  • Protease-activated receptor-2 (PAR-2) activation was involved in tryptase-induced inflammatory mediator release and mitochondrial dysfunction.
  • Tryptase-induced microglia activation was mediated by ERK and p38 MAPK pathways and NF-kappa B activation via PAR-2.

Conclusions:

  • Tryptase induces microglia activation and pro-inflammatory mediator release through the PAR-2-MAPK-NF-kappa B signaling pathway.
  • This mechanism contributes to the development of microglia-mediated inflammation in the brain.
  • Targeting this pathway may offer therapeutic strategies for neuroinflammatory conditions.

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