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首页> 美国卫生研究院文献>Immunology >The Candida albicans phospholipomannan induces in vitro production of tumour necrosis factor-alpha from human and murine macrophages.
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The Candida albicans phospholipomannan induces in vitro production of tumour necrosis factor-alpha from human and murine macrophages.

机译：白色念珠菌磷酸脂甘露聚糖诱导人和鼠巨噬细胞体外产生肿瘤坏死因子-α。

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摘要

We have previously identified a Candida albicans 14,000-18,000 MW antigen reacting with anti-beta-1,2-linked oligomannosides antibodies as being a phospholipomannan (PLM). Because of the structural similarities between the C. albicans PLM and lipophosphoglycans from various microbial pathogens known to be potent tumour necrosis factor-alpha (TNF-alpha) inducers, we investigated the PLM ability to induce TNF-alpha. Incubation of human monocytic cells THP-1 with PLM led to dose-dependent production of TNF-alpha that was significantly increased by prestimulation of the cells with interferon-gamma (IFN-gamma). Production of TNF-alpha by macrophages under PLM stimulation was confirmed by using macrophages elicited from the mouse peritoneal cavity. In all investigated conditions, PLM-induced TNF-alpha production differed significantly in both kinetics and dose dependence from lipopolysaccharide (LPS) induction used as control. It appears, therefore, that the C. albicans PLM shares functional homologies with microbial lipophosphoglycans identified as pathogenicity factors, although prestimulation of the target cells was required for the PLM-derived opportunistic pathogen to trigger the cytokine network.
机译：我们先前已经确定与抗β-1，2，连接的寡甘露糖苷抗体反应的白色念珠菌14,000-18,000 MW抗原是磷脂酰甘露聚糖（PLM）。由于白色念珠菌PLM与来自各种微生物病原体的脂磷酸聚糖之间的结构相似性，已知这些微生物病原体是有效的肿瘤坏死因子-α（TNF-alpha）诱导剂，我们研究了PLM诱导TNF-α的能力。将人单核细胞THP-1与PLM一起孵育会导致TNF-α的剂量依赖性产生，这种干扰可通过用干扰素-γ（IFN-γ）预先刺激细胞而显着增加。通过使用从小鼠腹膜腔诱发的巨噬细胞，证实了巨噬细胞在PLM刺激下产生TNF-α。在所有研究的条件下，PLM诱导的TNF-α产生的动力学和剂量依赖性均与用作对照的脂多糖（LPS）诱导显着不同。因此，白色念珠菌PLM与微生物脂质磷酸聚糖具有相同的功能同源性，而微生物脂磷脂聚糖被确定为致病因素，尽管PLM衍生的机会性病原体需要预先刺激靶细胞才能触发细胞因子网络。

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