Normal human gingival epithelial cells sense C. parapsilosis by toll-like receptors and module its pathogenesis through antimicrobial peptides and proinflammatory cytokines.

Normal human gingival epithelial cells sense C. parapsilosis by toll-like receptors and module its pathogenesis through antimicrobial peptides and proinflammatory cytokines.
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DOI:
10.1155/2010/940383
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发表时间:
2010
影响因子:
4.6
通讯作者:
Rouabhia M
Rouabhia M
中科院分区:
医学3区
文献类型:
--
作者:
Bahri R;Curt S;Saidane-Mosbahi D;Rouabhia M

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本研究旨在探讨C.使用单层培养物和工程化的人口腔粘膜(EHOM)对近平滑和人上皮细胞进行了研究。C.近平滑体能够粘附于牙龈上皮细胞,并在血清存在下采用菌丝形式。有趣的是,当在工程化的人口腔粘膜(EHOM)上培养时,C。近平滑形成小的生物膜并侵入结缔组织。与C接触后。正常人牙龈上皮细胞表达高水平的Toll样受体(TLR)-2、-4和-6,但不表达TLR-9 mRNA。IL-1β、TNFα和IFNγ mRNA表达的增加抑制了TLR的上调,提示这些细胞因子参与了对C.近平滑上皮细胞在抗念珠菌先天免疫中的积极作用。近平滑体感染通过它们表达高水平的人β-防御素-1、-2和-3的能力而增强。促炎细胞因子和抗菌肽表达的上调可能解释了C.牙龈上皮细胞增生。总体结果提供了上皮细胞参与抗C.近平滑感染
This study was designed to investigate the interaction between C. parapsilosis and human epithelial cells using monolayer cultures and an engineered human oral mucosa (EHOM). C. parapsilosis was able to adhere to gingival epithelial cells and to adopt the hyphal form in the presence of serum. Interestingly, when cultured onto the engineered human oral mucosa (EHOM), C. parapsilosis formed small biofilm and invaded the connective tissue. Following contact with C. parapsilosis, normal human gingival epithelial cells expressed high levels of Toll-like receptors (TLR)-2, -4, and -6, but not TLR-9 mRNA. The upregulation of TLRs was paralleled by an increase of IL-1β, TNFα, and IFNγ mRNA expression, suggesting the involvement of these cytokines in the defense against infection with C. parapsilosis. The active role of epithelial cells in the innate immunity against C. parapsilosis infection was enhanced by their capacity to express high levels of human beta-defensin-1, -2, and -3. The upregulation of proinflammatory cytokines and antimicrobial peptide expression may explain the growth inhibition of C. parapsilosis by the gingival epithelial cells. Overall results provide additional evidence of the involvement of epithelial cells in the innate immunity against C. parapsilosis infections.
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