Jouault T, Bernigaud A, Lepage G, Trinel P A, Poulain D
Unité INSERM 42, Domaine du CERTIA, Villeneuve d'Ascq, France.
Immunology. 1994 Oct;83(2):268-73.
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.
我们之前已鉴定出一种分子量为14,000 - 18,000道尔顿的白色念珠菌抗原，它能与抗β-1,2-连接的低聚甘露糖抗体发生反应，该抗原为磷脂甘露聚糖（PLM）。鉴于白色念珠菌PLM与已知为强效肿瘤坏死因子-α（TNF-α）诱导剂的各种微生物病原体的脂磷壁酸之间存在结构相似性，我们研究了PLM诱导TNF-α的能力。用PLM孵育人单核细胞THP-1导致TNF-α的剂量依赖性产生，在用干扰素-γ（IFN-γ）对细胞进行预刺激后，TNF-α的产生显著增加。通过使用从小鼠腹腔引出的巨噬细胞，证实了在PLM刺激下巨噬细胞产生TNF-α。在所有研究条件下，PLM诱导的TNF-α产生在动力学和剂量依赖性方面与用作对照的脂多糖（LPS）诱导均有显著差异。因此，尽管PLM衍生的机会性病原体需要对靶细胞进行预刺激才能触发细胞因子网络，但白色念珠菌PLM与被鉴定为致病因子的微生物脂磷壁酸具有功能同源性。
