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首页> 外文期刊>Infection and immunity >Antipyretic activity of a human immunoglobulin preparation for intravenous use in an experimental model of fever in rabbits.
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Antipyretic activity of a human immunoglobulin preparation for intravenous use in an experimental model of fever in rabbits.

机译：在兔发烧的实验模型中静脉内使用的人免疫球蛋白制剂的解热活性。

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In an effort to elucidate the reason that fever in patients with severe bacterial infections subsided in some cases after the administration of human immunoglobulin preparations for intravenous use (IGIVs), we focused our attention on the antipyretic activity of IGIVs by investigating experimentally produced pyrexia in rabbits with Escherichia coli-derived lipopolysaccharide (LPS). Although little difference in antibody titers against the antigens composing molecules of LPS was found among the IGIVs that were used, IGIVs treated at pH 4 were demonstrated to inhibit a strongly LPS-induced second-phase febrile response, whereas the inhibitory effect of sulfonated and pepsin-treated IGIVs was weak. In vitro experiments on interleukin-1 production by rabbit macrophages stimulated with LPS, silica gel or latex beads and on rosette formation showed that these functions of the cells were also inhibited by IGIVs. The in vivo antipyretic activity and the results of the two in vitro experiments correlated closely. The inhibitory potency decreased in the following order: immunoglobulin G (IgG) treated at pH4, sulfonated IgG, and pepsin-treated IgG. Thus, it is possible that the subsidence of LPS-induced fever by IGIVs was mediated by inhibition of interleukin 1 production by means of binding of IgG to macrophages via an Fc receptor. Results of this study also indicated the importance of the structural integrity of the Fc portion of the IgG contained in the IGIVs to bind with its receptor on the macrophage so as to influence the various functions carried out by the cell.
机译：为了阐明在使用静脉注射人免疫球蛋白制剂（IGIV）后某些情况下严重细菌感染患者的发烧平息的原因，我们通过研究家兔实验产生的发热来集中注意力于IGIV的解热活性。含大肠杆菌衍生的脂多糖（LPS）。尽管在使用的IGIV中发现针对组成LPS分子的抗原的抗体效价差异不大，但已证明在pH 4下处理的IGIV抑制了LPS诱导的第二阶段高热反应，而磺化和胃蛋白酶的抑制作用治疗的IGIV较弱。体外实验对LPS，硅胶或乳胶珠刺激的兔巨噬细胞产生白介素-1以及玫瑰花结的形成表明，IGIV也可抑制细胞的这些功能。体内的解热活性与两个体外实验的结果密切相关。抑制力按以下顺序降低：在pH4下处理的免疫球蛋白G（IgG），磺化IgG和胃蛋白酶处理的IgG。因此，通过IgG通过Fc受体与巨噬细胞结合，通过抑制白介素1的产生来介导IGIV引起的LPS诱导的发热的下陷。这项研究的结果还表明，IGIV中包含的IgG的Fc部分与其在巨噬细胞上的受体结合从而影响细胞所执行的各种功能的结构完整性的重要性。

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