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小鼠实验性感染脑心肌炎(EMC)病毒对体外肺泡细胞和腹腔细胞产生干扰素的影响。

The effect of experimental infection of mice with encephalomyocarditis (EMC) virus on interferon production by alveolar and peritoneal cells in vitro.

作者信息

Lobodzińska M, Albin M, Skurska Z

出版信息

Arch Immunol Ther Exp (Warsz). 1981;29(1):91-5.

PMID:6169322
Abstract

After infection of mice with EMC virus, dose-dependent increase or decrease of the synthesis of in vitro Newcastle disease virus (NDV)-induced interferon was observed in alveolar and peritoneal cells. It was shown that peritoneal cells from mice with mild course of the infection (infecting dose 0.2-1.0 LD50 per mouse) produce interferon in vitro on the same level as the control cells. Alveolar cells isolated from the same mice shortly after infection exhibited increased interferon production in vitro as compared with the analogous cells isolated from the non-infected mice. Acute, EMC-induced infection in mice (infecting dose 5.0 LD50 per mouse) caused suppression of interferon synthesis in vitro by both peritoneal and alveolar cells, which intensified together with the progression of the disease.

摘要

用脑心肌炎病毒感染小鼠后,在肺泡细胞和腹腔细胞中观察到体外新城疫病毒(NDV)诱导的干扰素合成呈剂量依赖性增加或减少。结果表明,感染病程较轻的小鼠(每只小鼠感染剂量为0.2 - 1.0 LD50)的腹腔细胞在体外产生干扰素的水平与对照细胞相同。感染后不久从同一小鼠分离的肺泡细胞与从未感染小鼠分离的类似细胞相比,体外干扰素产生增加。小鼠急性脑心肌炎病毒诱导的感染(每只小鼠感染剂量为5.0 LD50)导致腹腔细胞和肺泡细胞体外干扰素合成受到抑制,且随着疾病进展这种抑制加剧。

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