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A critical role of Dectin-1 in hypersensitivity pneumonitis

Mari Higashino-Kameda1,2, Toshiki Yabe-Wada2, Shintaro Matsuba2

  • 1Department of Respiratory Medicine, Kanazawa Medical University, Uchinada, Ishikawa, Japan.

Inflammation Research : Official Journal of the European Histamine Research Society ... [Et Al.]
|December 9, 2015
PubMed
Abstract

Insights

Dectin-1 is critical for developing hypersensitivity pneumonitis (HP) caused by the fungus Trichosporon asahii. Dectin-1 deficiency prevented HP development in mice, highlighting its role in this fungal lung disease.

Area of Science:

  • Immunology
  • Pulmonology
  • Mycology

Background:

  • Hypersensitivity pneumonitis (HP) is a lung disease from inhaling antigens like fungi.
  • Toll-like receptors (TLRs) are involved in bacterial HP, but fungal receptor roles are unclear.
  • Summer-type HP is linked to Trichosporon asahii fungus.

Purpose of the Study:

  • To investigate the role of Dectin-1 and Dectin-2 in experimental HP induced by Trichosporon asahii.
  • To determine if these fungal receptors are crucial for developing fungus-induced HP.

Main Methods:

  • Binding assays of Dectin-Fc protein with T. asahii.
  • Histological and flow cytometric analysis in Dectin-1-deficient and Dectin-2-deficient mice.
  • Analysis of Th17/Th1 responses and IL-23 production in lung cells and bone marrow-derived dendritic cells.

Main Results:

  • Dectin-1 showed stronger binding to T. asahii than Dectin-2.
  • Dectin-1-deficient mice exhibited significantly reduced HP development compared to wild-type and Dectin-2-deficient mice.
  • Dectin-1 deficiency led to decreased neutrophil and macrophage infiltration, reduced CD4(+)IL-17A(+) cell expansion, and lower IL-23 production.

Conclusions:

  • Dectin-1 plays a critical role in the pathogenesis of fungus-induced hypersensitivity pneumonitis.
  • Targeting Dectin-1 may offer a therapeutic strategy for HP caused by fungal antigens.
Keywords:
Dectin-1Hypersensitivity pneumonitisTh17Trichosporon asahii

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