Induction of tumor necrosis factor production from monocytes stimulated with mannuronic acid polymers and involvement of lipopolysaccharide-binding protein, CD14, and bactericidal/permeability-increasing factor
Induction of tumor necrosis factor production from monocytes stimulated with mannuronic acid polymers and involvement of lipopolysaccharide-binding protein, CD14, and bactericidal/permeability-increasing factor
复制标题
DOI：
10.1128/iai.65.1.89-94.1997
复制
发表时间：
1997-01
影响因子：
3.1
通讯作者：
T. G. Jahr;L. Ryan;A. Sundan;Henri S. Lichenstein;G. Skjåk-Bræk;T. Espevik
中科院分区：
文献类型：
--
作者：
T. G. Jahr;L. Ryan;A. Sundan;Henri S. Lichenstein;G. Skjåk-Bræk;T. Espevik
明确定义的多糖，如来源于铜绿假单胞菌的β 1 -4-连接的D-甘露糖醛酸（poly[M]），通过涉及膜CD 1 - 4的途径诱导单核细胞产生肿瘤坏死因子（TNF）。在这项研究中，我们研究了可溶性CD 14（sCD 14），脂多糖结合蛋白（LBP），杀菌/渗透性增加因子（BPI）对多聚（M）结合单核细胞和诱导TNF产生的影响。我们发现LBP增加了用poly（M）刺激的单核细胞的TNF产生。单独添加sCD 14仅具有微小的影响，但当其与LBP一起添加时，观察到TNF产生的增加。发现BPI抑制在LBP、LBP-sCD 14或10%人血清存在下用poly（M）刺激的单核细胞的TNF产生。结合研究表明，poly（M）与LBP和BPI包被的免疫细胞结合，而在没有血清的情况下，没有观察到poly（M）与sCD 14包被的威尔斯孔的显著结合。还通过流式细胞术检测了聚（M）与单核细胞的结合，并且显示添加LBP或10%人血清明显增加了聚（M）与单核细胞的结合。在LBP、LBP-sCD 14或10%人血清存在下，BPI抑制poly（M）与单核细胞的结合。我们的数据证明了LBP、LBP-sCD 14和BPI在调节确定的多糖的TNF应答中的作用。
Well-defined polysaccharides, such as beta1-4-linked D-mannuronic acid (poly[M]) derived from Pseudomonas aeruginosa, induce monocytes to produce tumor necrosis factor (TNF) through a pathway involving membrane CD14. In this study we have investigated the effects of soluble CD14 (sCD14), lipopolysaccharide-binding protein (LBP), and bactericidal/permeability-increasing factor (BPI) on poly(M) binding to monocytes and induction of TNF production. We show that LBP increased the TNF production from monocytes stimulated with poly(M). Addition of sCD14 alone had only minor effects, but when it was added together with LBP, a rise in TNF production was seen. BPI was found to inhibit TNF production from monocytes stimulated with poly(M) in the presence of LBP, LBP-sCD14, or 10% human serum. Binding studies showed that poly(M) bound to LBP- and BPI-coated immunowells, while no significant binding of poly(M) to sCD14-coated wells in the absence of serum was observed. Binding of poly(M) to monocytes was also examined by flow cytometry, and it was shown that the addition of LBP or 10% human serum clearly increased the binding of poly(M) to monocytes. BPI inhibited the binding of poly(M) to monocytes in the presence of LBP, LBP-sCD14, or 10% human serum. Our data demonstrate a role for LBP, LBP-sCD14, and BPI in modulating TNF responses of defined polysaccharides.