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Insoluble β-glucan from the cell wall of Candida albicans induces immune responses of human THP-1 monocytes through Dectin-1

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Author:
No author available
Journal Title:
CHINESE MEDICAL JOURNAL
Issue:
5
DOI:
10.3760/cma.j.issn.0366-6999.2009.05.003
Key Word:
Candida albicans;monocytes;insoluble β-glucan;Dectin-1;cytokines;hydrogen peroxide

Abstract: Background β-glucan is the major structure component of Candida albicans (C. albicans) cell wall. It has been demonstrated that Dectin-1 as the principal C-type lectin pattern-recognition receptor (PRR) can recognize fungal β-glucan and induce immune responses. In this study, we sought to clarify whether insoluble β-glucan from the cell wall of C. albicans (CalG) could induce immune responses in human THP-1 monocytes (a human acute monocytic leukemia cell line) and to determine the underlying mechanisms.Methods Human THP-1 monocytes were challenged with CalG in vitro. The mRNA expression of Dectin-1, Toll-like receptors (TLR2), proinflammatory cytokine (TNF-α) and chemokine (IL-8) was assayed by real-time reverse transcription polymerase chain reaction (RT-PCR). The secretion of TNF-α and IL-8 were measured by enzyme-linked immunosorbent assay (ELISA). H2O2 release was determined by microplate fluorescent assay. Western blotting was used to analyze IkB-α phosphorylation and degradation.Results Exposure of THP-1 monocytes to CalG led to increased gene expression and secretion of TNF-α and IL-8.CalG induced H2O2 release in a time-dependent manner. CalG hydrolyzed with zymolyase failed to induce gene expression and secretion of TNF-α, IL-8 and H2O2 release. CalG up-regulated the mRNA of Dectin-1, whereas the mRNA level of TLR2 was not altered. THP-1 monocytes challenged with CalG resulted in the activation of NF-KB in a time-dependent manner. Dectin-1 inhibitor laminarin blocked the CalG-induced production of TNF-α and H2O2 in THP-1 monocytes, but no such effect was observed in pretreatment with anti-TLR2 neutralizing antibody and the LPS inhibitor (polymyxin B).Conclusion CalG may play a role in activation of immune responses in human THP-1 cells through Dectin-1, not TLR2.This work was supported by a grant from National Natural ScienceFoundation of China (No. 30671893).

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