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首页> 外文期刊>Journal of Hepatology: The Journal of the European Association for the Study of the Liver >Inhibition of concanavalin A-induced hepatic injury of mice by bacterial lipopolysaccharide via the induction of IL-6 and the subsequent reduction of IL-4: the cytokine milieu of concanavalin A hepatitis.
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Inhibition of concanavalin A-induced hepatic injury of mice by bacterial lipopolysaccharide via the induction of IL-6 and the subsequent reduction of IL-4: the cytokine milieu of concanavalin A hepatitis.

机译：细菌脂多糖通过诱导IL-6并随后降低IL-4抑制刀豆球蛋白A诱导的小鼠肝损伤：刀豆球蛋白A肝炎的细胞因子环境。

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BACKGROUND/AIMS: Liver natural killer 1.1 antigen (NK1)+ T cells and IL-4 play a crucial role in concanavalin-A (Con-A)-induced hepatic injury in mice, and a T helper (Th) 2 immune response was thus suggested to be involved. This study was designed to examine the effect of bacterial lipopolysaccharide (LPS), a strong inducer of a Th 1 immune response, on Con-A hepatic injury and also to clarify further the cytokine milieu of Con-A hepatitis. Methods: LPS were injected into mice before Con-A injection to evaluate the effect on hepatic injury. The effect of the pretreatment with various T1 and Th2 cytokines or anti-cytokine antibodies on Con-A hepatitis was also examined. Results: LPS in quantities > or = 500 ng/mouse, when injected 24 h before Con-A injection, abrogated the Con-A-induced elevation of transaminases, hepatocyte destruction and serum IL-4 elevation. This LPS inhibitory effect was blocked when the mice were injected with either anti-IL-6 antibody before LPS injection or IL-4 before Con-A injection. IL-6, but neither IL-10 nor IL-12 pretreatment suppressed Con-A-induced IL-4 production and hepatitis. NK1+ T cells produced IL-4 while both NK1+ T cells and NK1- T cells produced IFN-gamma. Not only anti-IL-4 antibody but also the anti-IFN-gamma antibody pretreatment inhibited Con-A hepatitis. However, although the anti-IL4 antibody suppressed IL-4 alone, the anti-IFN-gamma Ab unexpectedly inhibited both IFN-gamma and IL-4 elevation, while IL-4 injection evoked a moderate Con-A hepatitis even in the anti-IFN-gamma antibody-treated mice. Furthermore, the IL-4 mutant mice did not develop Con-A hepatitis. CONCLUSION: LPS inhibited Con-A hepatitis by inducing IL-6 and thereby inhibited IL-4 synthesis from NK1+ T cells. Although both IL-4 and IFN-gamma were required for the full induction of Con-A hepatic injury, exogenous IL-4 evoked a moderate Con-A hepatitis, even in the absence of IFN-gamma.
机译：背景/目的：肝自然杀手1.1抗原（NK1）+ T细胞和IL-4在伴刀豆球蛋白A（Con-A）诱导的小鼠肝损伤中起关键作用，而T辅助（Th）2免疫应答为因此建议参与其中。这项研究旨在检查细菌脂多糖（LPS）（一种Th 1免疫应答的强诱导剂）对Con-A肝损伤的作用，并进一步阐明Con-A肝炎的细胞因子环境。方法：在Con-A注射之前，将LPS注射入小鼠，以评估其对肝损伤的作用。还检查了用各种T1和Th2细胞因子或抗细胞因子抗体进行预处理对Con-A肝炎的影响。结果：当在Con-A注射前24小时注射LPS≥500 ng /小鼠时，可消除Con-A引起的转氨酶升高，肝细胞破坏和血清IL-4升高。当在LPS注射之前向小鼠注射抗IL-6抗体或在Con-A注射之前向小鼠注射IL-4时，这种LPS抑制作用被阻断。 IL-6，但IL-10和IL-12预处理均不能抑制Con-A诱导的IL-4产生和肝炎。 NK1 + T细胞产生IL-4，而NK1 + T细胞和NK1-T细胞都产生IFN-γ。不仅抗IL-4抗体而且抗IFN-γ抗体预处理均抑制Con-A肝炎。但是，尽管抗IL4抗体仅抑制IL-4，但抗IFN-γAb却出人意料地抑制了IFN-γ和IL-4的升高，而IL-4注射甚至引起了中度Con-A肝炎IFN-γ抗体治疗的小鼠。此外，IL-4突变小鼠没有患上Con-A肝炎。结论：脂多糖通过诱导IL-6抑制Con-A肝炎，从而抑制NK1 + T细胞的IL-4合成。尽管完全诱导Con-A肝损伤需要IL-4和IFN-γ，但是即使没有IFN-γ，外源性IL-4也会引起中度Con-A肝炎。

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