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

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 wh...

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Bibliographic Details
Published in:Chinese medical journal 2009-03, Vol.122 (5), p.496-501
Main Authors: Li, Min, Liu, Ze-hu, Chen, Qing, Zhou, Wu-qing, Yu, Mei-wen, Lü, Gui-xia, Lü, Xue-lian, Shen, Yong-nian, Liu, Wei-da, Wu, Shao-xi
Format: Article
Language:English
Subjects:
beta-Glucans - pharmacology
Blotting, Western
Candida albicans - metabolism
Cell Line, Tumor
Cell Wall - metabolism
Enzyme-Linked Immunosorbent Assay
Gene Expression - drug effects
Humans
Hydrogen Peroxide - metabolism
Interleukin-8 - genetics
Interleukin-8 - metabolism
Lectins, C-Type
Membrane Proteins - genetics
Membrane Proteins - metabolism
Monocytes - drug effects
Monocytes - immunology
Monocytes - metabolism
Nerve Tissue Proteins - genetics
Nerve Tissue Proteins - metabolism
Reverse Transcriptase Polymerase Chain Reaction
THP
Toll-Like Receptor 2 - genetics
Tumor Necrosis Factor-alpha - genetics
Tumor Necrosis Factor-alpha - metabolism
不溶性
免疫反应
实时逆转录聚合酶链反应
急性单核细胞
白色念珠菌
细胞壁
葡聚糖
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Summary: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-a） and chemokine （IL-8） was assayed by real-time reverse transcription polymerase chain reaction （RT-PCR）. The secretion of TNF-a 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-a phosphorylation and degradation. Results Exposure of THP-1 monocytes to CalG led to increased gene expression and secretion of TNF-a 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-a, 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-a 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 throuah Dectin-1, not TLR2.
ISSN:0366-6999
2542-5641
DOI:10.3760/cma.j.issn.0366-6999.2009.05.003