Related Experiment Video

Updated: May 2, 2026

Infecting Mice with Malassezia spp. to Study the Fungus-Host Interaction
06:19

Infecting Mice with Malassezia spp. to Study the Fungus-Host Interaction

Published on: November 6, 2019

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PAR2-β-arrestin 2-ERK axis mediates Malassezia globosa-induced IL-17 response by disrupting ZO-1 in keratinocytes

Jinfeng Tang1,2, Fanggu Li2, Jiaqing Hong2

  • 1Clinical Research Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China.

Iscience
|May 1, 2026
PubMed

Insights

Protease-activated receptor 2 (PAR2) plays a key role in Malassezia infections by disrupting skin barrier proteins and amplifying inflammation. Targeting PAR2 offers a potential therapeutic strategy for Malassezia-related skin diseases.

Area of Science:

  • Dermatology
  • Mycology
  • Immunology

Background:

  • Malassezia yeast is a common skin commensal that can act as an opportunistic pathogen.
  • The role of protease-activated receptor 2 (PAR2) in Malassezia-related skin conditions is not well understood.

Purpose of the Study:

  • To investigate the specific role of PAR2 in the pathogenesis of Malassezia infections.
  • To elucidate the molecular mechanisms by which Malassezia interacts with host cells via PAR2.

Main Methods:

  • Co-immunoprecipitation (Co-IP), proximity ligation assay (PLA), and Malassezia-yeast interaction assays.
  • Analysis of Malassezia folliculitis patient samples, cell culture infection models, and murine infection models.

Main Results:

  • PAR2 was found to interact with Zonula occludens-1 (ZO-1) and beta-arrestin 2 in Malassezia-infected keratinocytes.
  • Malassezia globosa exploits the PAR2-beta-arrestin 2-ERK signaling pathway, disrupting ZO-1 and increasing IL-17 inflammation.
  • Inhibition or genetic deletion of PAR2 reduced Malassezia-induced IL-17 inflammation.

Conclusions:

  • PAR2 is a critical mediator of Malassezia-induced inflammation.
  • PAR2 represents a potential therapeutic target for treating Malassezia-related diseases.
  • This study provides new insights into the pathogenic mechanisms of commensal fungi.
Keywords:
Cell biologyImmunologyMolecular biology

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