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首页> 外文期刊>Infection and immunity >Differential Cytokine Production and Toll-Like Receptor Signaling Pathways by Candida albicans Blastoconidia and Hyphae
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Differential Cytokine Production and Toll-Like Receptor Signaling Pathways by Candida albicans Blastoconidia and Hyphae

机译：念珠菌念珠菌和菌丝的差异性细胞因子生产和类似收费的信号通路。

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摘要

Toll-like receptors (TLR) are crucial for an efficient antifungal defense. We investigated the differential recognition of blastoconidia and hyphae of Candida albicans by TLRs. In contrast to Candida blastoconidia, which stimulated large amounts of gamma interferon (IFN-γ), the tissue-invasive Candida hyphae did not stimulate any IFN-γ by human peripheral blood mononuclear cells (PBMC) or murine splenic lymphocytes. After stimulation with blastoconidia, the production of IFN-γ was TLR4 dependent, as shown by the significantly decreased IFN-γ production in anti-TLR4-treated PBMC and in splenic lymphocytes from TLR4-defective ScCr mice. In addition, peritoneal macrophages from ScCr mice produced less tumor necrosis factor α (TNF-α) than macrophages of control mice did when stimulated with Candida blastoconidia, but not with hyphae, indicating that TLR4-mediated signals are lost during hyphal germination. In contrast, macrophages from TLR2 knockout mice had a decreased production of TNF-α in response to both Candida blastoconidia and hyphae. Candida hyphae stimulated production of interleukin-10 through TLR2-dependent mechanisms. In conclusion, TLR4 mediates proinflammatory cytokine induction after Candida stimulation, whereas Candida recognition by TLR2 leads mainly to anti-inflammatory cytokine release. TLR4-mediated proinflammatory signals are lost during germination of Candida blastoconidia into hyphae. Phenotypic switching during germination may be an important escape mechanism of C. albicans, resulting in counteracting host defense.
机译：Toll样受体（TLR）对于有效的抗真菌防御至关重要。我们研究了TLRs对白色念珠菌的胚芽孢杆菌和菌丝的区别识别。与刺激大量γ-干扰素（IFN-γ）的 Candida blastoconidia相比，组织侵袭性 Candida 菌丝不刺激人外周血中的任何IFN-γ单核细胞（PBMC）或鼠脾淋巴细胞。在产气过劲病刺激后，IFN-γ的产生是TLR4依赖性的，如抗TLR4处理的PBMC和TLR4缺陷的ScCr小鼠的脾脏淋巴细胞的IFN-γ产生显着降低所示。此外，当用 Candida blastoconidia刺激时，ScCr小鼠的腹膜巨噬细胞产生的肿瘤坏死因子α（TNF-α）比对照小鼠的巨噬细胞要少，但没有被菌丝刺激，这表明TLR4介导的信号是在菌丝萌发过程中丢失。相比之下，TLR2基因敲除小鼠的巨噬细胞对 Candida blastoconidia和菌丝均具有降低的TNF-α产生。 Candida 菌丝通过TLR2依赖性机制刺激白介素10的产生。总之，在 Candida 刺激后，TLR4介导促炎性细胞因子的诱导，而TLR2对 Candida 的识别主要导致抗炎性细胞因子的释放。在 Candida blastoconidia发芽到菌丝中时，TLR4介导的促炎信号丢失。发芽过程中的表型转换可能是 C的重要逃逸机制。白色的，从而抵消了宿主的防御能力。

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