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Int. J. Mol. Sci. 2017, 18(3), 624; doi:10.3390/ijms18030624

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

1
Department of Obstetrics and Gynecology, Taipei Veterans General Hospital, Taipei 112, Taiwan
2
Institute of Clinical Medicine, National Yang-Ming University, Taipei 112, Taiwan
3
Department of Obstetrics and Gynecology, National Yang-Ming University, Taipei 112, Taiwan
4
Institute of BioMedical Informatics, National Yang-Ming University, Taipei 112, Taiwan
5
Department of Medical Research, Taipei Veterans General Hospital, Taipei 112, Taiwan
6
Genomics Research Center, Academia Sinica, Taipei 11529, Taiwan
7
Department of Medical Research, China Medical University Hospital, Taichung 40447, Taiwan
*
Author to whom correspondence should be addressed.
Academic Editors: Paul R. Reynolds and Benjamin T. Bikman
Received: 12 January 2017 / Revised: 7 March 2017 / Accepted: 10 March 2017 / Published: 13 March 2017
(This article belongs to the Special Issue Inhaled Pollutants Modulate Respiratory and Systemic Diseases)
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Abstract

Fusarium species are causative agents of human respiratory disorders and are distributed widely in our environment. Little is known of their interaction with human respiratory epithelial cells, which may contribute to allergic airway responses. In this study, we report on the release of C–X–C motif chemokine ligand 8 (CXCL-8) from human bronchial epithelial BEAS-2B cells upon stimulation with Fusarium proliferatum extracts. F. proliferatum-induced cytokine release from BEAS-2B cells was determined by cytokine array and CXCL-8 enzyme-linked immunosorbent assay (ELISA) kits. Blocking antibodies and signaling pathway inhibitors were employed to delineate cell surface receptors and signaling pathways participating in CXCL-8 release. F. proliferatum extracts induced the release of CXCL-8 in a time-dependent manner. The dectin-1 receptor ligands, curdlan and laminarin, reduced CXCL-8 release. Cells pre-treated with anti-Dectin-1 antibodies (2 µg/mL) decreased CXCL-8 release by 24%. Furthermore, F. proliferatum-stimulated CXCL-8 release was reduced by 32%, 53%–81%, 40% and 26% after BEAS-2B cells were pretreated with activation inhibitors of spleen tyrosine kinase (Syk)—piceatannol—, mitogen-activated protein kinases (MAPKs)—PD98059, U0126, SB202190, SP600125—, phosphatidylinositol-3-kinase (PI3K)—LY294002—and nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB)—BAY117082—, respectively. These results suggest that Dectin-1-mediated activation of the Syk, MAPKs, PI3K and NF-κB signaling pathways contributes to F. proliferatum-stimulated CXCL-8 release from BEAS-2B cells and provides an important basis for developing novel therapeutic strategies in clinical allergy. View Full-Text
Keywords: Fusarium proliferatum; CXCL-8; respiratory epithelial cells; Dectin-1 Fusarium proliferatum; CXCL-8; respiratory epithelial cells; Dectin-1
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MDPI and ACS Style

Yeh, C.-C.; Horng, H.-C.; Chou, H.; Tai, H.-Y.; Shen, H.-D.; Hsieh, S.-L.; Wang, P.-H. Dectin-1-Mediated Pathway Contributes to Fusarium proliferatum-Induced CXCL-8 Release from Human Respiratory Epithelial Cells. Int. J. Mol. Sci. 2017, 18, 624.

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