溶菌酶调节lps诱导的小鼠白介素-6释放。

Circulatory shock Pub Date : 1994-12-01
K Takada, N Ohno, T Yadomae
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引用次数: 0

摘要

细菌脂多糖(LPS)刺激内源性介质(如肿瘤坏死因子(TNF)、白细胞介素-1和-6 (IL-1和IL-6)、血小板活化因子(PAF))的产生和释放,导致脓毒症的病理生理变化和死亡率。我们最近证明了与LPS结合的溶菌酶(LZM-LPS复合物)在体内抑制LPS诱导的肿瘤坏死因子- α (tnf - α)的产生。在本研究中,我们在体外和体内研究了LZM-LPS复合物形成对lps诱导的IL-6产生的影响。添加LZM-LPS复合物后,小鼠巨噬细胞样细胞RAW264.7中tnf - α和IL-6的释放明显低于LPS,且呈剂量依赖性。carrageenan (CAR)引物小鼠血清中LPS产生的IL-6在注射后2小时达到峰值。LZM-LPS和lzm -大肠杆菌细胞复合物(每只小鼠1微克LPS)释放的血清IL-6浓度显著降低(与car预处理的LPS或细胞注射的小鼠相比,P < 0.01和P < 0.001)。这些结果强调了LZM在体内中和内毒素中的重要作用。然而,在IL-6的情况下,通过施用致死剂量的LPS(每只小鼠100微克LPS), LZM降低了IL-6的水平,但仍释放出显著浓度的IL-6;尽管TNF- α浓度在本实验条件下可以忽略不计。因此,提示LZM可能通过抑制血清中细胞因子的释放来调节革兰氏阴性菌感染引起的全身炎症。
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Lysozyme regulates LPS-induced interleukin-6 release in mice.

Bacterial lipopolysaccharide (LPS) stimulates the production and release of endogenous mediators [e.g., tumor necrosis factor (TNF), interleukins-1 and -6 (IL-1 and IL-6), and Platelet Activating Factor [PAF] responsible for the pathophysiologic changes and the mortality associated with sepsis. We recently demonstrated that lysozyme (LZM) bound to LPS (LZM-LPS complex) suppresses LPS-induced tumor necrosis factor-alpha (TNF-alpha) production in vivo. In the present study, we investigated the effect of LZM-LPS complex formation on LPS-induced IL-6 production, both in vitro and in vivo. With the addition of LZM-LPS complex, TNF-alpha and IL-6 release was significantly reduced compared with that by LPS in a dose-dependent manner in mouse macrophage-like cells, RAW264.7. IL-6 production in serum by LPS in carrageenan (CAR)-primed mice peaked at 2 hr following injection. LZM-LPS and LZM-Escherichia coli cell complex (as 1 microgram of LPS per mouse) released significantly reduced concentrations of IL-6 in serum (P < 0.01 and P < 0.001 versus CAR-pretreated LPS- or cell-injected mice). These results emphasize the important role of LZM in vivo in the neutralization of endotoxin. However, in the case of IL-6, by administration of a lethal dose of LPS (as 100 micrograms of LPS per mouse), the IL-6 level was reduced by LZM, but a significant concentration of IL-6 was still released; although the TNF- alpha concentration was negligible in this experimental condition. Thus, it is suggested that LZM might regulate the systemic inflammation induced during Gram-negative bacterial infections by inhibiting the release of cytokines in serum.

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Comparison of binding specificity and the function of two human IgM anti-lipid A monoclonal antibodies. Hypertonic saline/dextran versus lactated Ringer's treatment for hemorrhage in dehydrated swine. Lysozyme regulates LPS-induced interleukin-6 release in mice. Liver oxygen uptake dependence and mitochondrial function in septic rats. Efficacy of continuous arteriovenous hemofiltration in endotoxic shock.
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