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Candida albicans phospholipomannan triggers inflammatory responses of human keratinocytes through Toll-like receptor 2.
Exp Dermatol. 2009 Jul; 18(7):603-10.ED

Abstract

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 beta-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-kappaB and mitogen-activated protein kinase (MAPKs) including p38. Anti-TLR2 neutralizing antibody, NFkappaB 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-kappaB and p38MAPK signalling pathway dependent manner.

Authors+Show Affiliations

Institute of Dermatology, Chinese Academy of Medical Science & Peking Union Medical College, 12 Jiangwangmiao St., Nanjing 210042, China. minli08@gmail.comNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

19196344

Citation

Li, Min, et al. "Candida Albicans Phospholipomannan Triggers Inflammatory Responses of Human Keratinocytes Through Toll-like Receptor 2." Experimental Dermatology, vol. 18, no. 7, 2009, pp. 603-10.
Li M, Chen Q, Shen Y, et al. Candida albicans phospholipomannan triggers inflammatory responses of human keratinocytes through Toll-like receptor 2. Exp Dermatol. 2009;18(7):603-10.
Li, M., Chen, Q., Shen, Y., & Liu, W. (2009). Candida albicans phospholipomannan triggers inflammatory responses of human keratinocytes through Toll-like receptor 2. Experimental Dermatology, 18(7), 603-10. https://doi.org/10.1111/j.1600-0625.2008.00832.x
Li M, et al. Candida Albicans Phospholipomannan Triggers Inflammatory Responses of Human Keratinocytes Through Toll-like Receptor 2. Exp Dermatol. 2009;18(7):603-10. PubMed PMID: 19196344.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Candida albicans phospholipomannan triggers inflammatory responses of human keratinocytes through Toll-like receptor 2. AU - Li,Min, AU - Chen,Qing, AU - Shen,Yongnian, AU - Liu,Weida, Y1 - 2008/12/19/ PY - 2009/2/7/entrez PY - 2009/2/7/pubmed PY - 2009/10/24/medline SP - 603 EP - 10 JF - Experimental dermatology JO - Exp Dermatol VL - 18 IS - 7 N2 - 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 beta-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-kappaB and mitogen-activated protein kinase (MAPKs) including p38. Anti-TLR2 neutralizing antibody, NFkappaB 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-kappaB and p38MAPK signalling pathway dependent manner. SN - 1600-0625 UR - https://www.unboundmedicine.com/medline/citation/19196344/Candida_albicans_phospholipomannan_triggers_inflammatory_responses_of_human_keratinocytes_through_Toll_like_receptor_2_ L2 - https://doi.org/10.1111/j.1600-0625.2008.00832.x DB - PRIME DP - Unbound Medicine ER -