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Dectin-1-Mediated Pathway Contributes to Fusarium proliferatum-Induced CXCL-8 Release from Human Respiratory

Chang-Ching Yeh1,2,3, Huann-Cheng Horng4,5,6, Hong Chou7

  • 1Department of Obstetrics and Gynecology, Taipei Veterans General Hospital, Taipei 112, Taiwan. ccyeh39@gmail.com.

International Journal of Molecular Sciences
|March 25, 2017
PubMed

Insights

Fusarium proliferatum fungal extracts trigger human airway cells to release CXCL-8, a key inflammatory mediator. This response involves Dectin-1 receptor activation and downstream signaling pathways, offering targets for allergy treatments.

Area of Science:

  • Immunology
  • Respiratory Medicine
  • Mycology

Background:

  • * Fusarium species are common environmental fungi implicated in human respiratory issues.
  • * The interaction between Fusarium and respiratory epithelial cells, particularly in allergic responses, is not well understood.
  • * C-X-C motif chemokine ligand 8 (CXCL-8) is a critical cytokine in airway inflammation.

Purpose of the Study:

  • * To investigate the release of CXCL-8 from human bronchial epithelial cells stimulated by Fusarium proliferatum.
  • * To identify the cell surface receptors and signaling pathways involved in this response.
  • * To provide a basis for developing new therapeutic strategies for clinical allergy.

Main Methods:

  • * Human bronchial epithelial BEAS-2B cells were stimulated with Fusarium proliferatum extracts.
  • * Cytokine arrays and CXCL-8 enzyme-linked immunosorbent assay (ELISA) kits were used for quantification.
  • * Blocking antibodies against Dectin-1 and inhibitors for Syk, MAPKs, PI3K, and NF-κB signaling pathways were employed.

Main Results:

  • * Fusarium proliferatum extracts induced a time-dependent release of CXCL-8 from BEAS-2B cells.
  • * Dectin-1 receptor engagement was implicated, as blocking antibodies reduced CXCL-8 release by 24%.
  • * Inhibition of Syk, MAPKs, PI3K, and NF-κB signaling pathways significantly reduced Fusarium-induced CXCL-8 release (26%-81%).

Conclusions:

  • * Dectin-1 receptor activation plays a crucial role in Fusarium-induced CXCL-8 release.
  • * The Syk, MAPKs, PI3K, and NF-κB signaling pathways are essential mediators of this inflammatory response.
  • * Targeting these pathways presents a potential therapeutic avenue for managing Fusarium-related allergic airway diseases.
Keywords:
CXCL-8Dectin-1Fusarium proliferatumrespiratory epithelial cells

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