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Candida albicans phospholipomannan triggers inflammatory responses of human keratinocytes through Toll‐like receptor 2
Author(s) -
Li Min,
Chen Qing,
Shen Yongnian,
Liu Weida
Publication year - 2009
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2008.00832.x
Subject(s) - tlr2 , candida albicans , proinflammatory cytokine , tlr4 , secretion , toll like receptor , biology , chemokine , innate immune system , corpus albicans , microbiology and biotechnology , inflammation , signal transduction , immunology , immune system , biochemistry
The Toll‐like receptors (TLRs) play an important role in the recognition of Candida albicans components and activation of innate immunity. Phospholipomannan (PLM), a glycolipid, is expressed at the surface of C. albicans cell wall, which acts as a member of the pathogen‐associated molecular patterns family. In this study, we sought to clarify whether C. albicans ‐native PLM could induce an inflammation response in human keratinocytes and to determine the underlying mechanisms. Exposure of cultured human primary keratinocytes to PLM led to the increased gene expression and secretion of proinflammatory cytokines (IL‐6) and chemokines (IL‐8). PLM hydrolysed with β‐ d ‐mannoside mannohydrolase failed to induce gene expression and secretion of IL‐6 and IL‐8. PLM up‐regulated the mRNA and protein levels of TLR2, whereas the mRNA level of TLR4 was not altered. Keratinocytes challenged with PLM resulted in the activation of NF‐κB and mitogen‐activated protein kinase (MAPKs) including p38. Anti‐TLR2 neutralizing antibody, NFκB and p38MAPK inhibitors blocked the PLM‐induced secretion of IL‐6, IL‐8 in keratinocytes, but no such effect was observed in pretreatment with anti‐TLR4‐neutralizing antibody and lipopolysaccharide inhibitor (polymyxin B). These data suggest C. albicans ‐native PLM may contribute to the inflammatory responses of cutaneous candidiasis in the TLR2‐NF‐κB and p38MAPK signalling pathway dependent manner.