Soldaini E, Baldinotti F, Matteucci D, Specter S, Bendinelli M
Department of Biomedicine, University of Pisa, Italy.
J Biol Regul Homeost Agents. 1994 Jan-Mar;8(1):25-31.
Friend leukemia virus complex (FLC) infection of BALB/c mice causes a rapid, progressive suppression of most immune functions. In the present study, FLC infection resulted in increased induction by bacterial lipopolysaccharide (LPS) of tumor necrosis factor alpha (TNF alpha) but not IL-6. TNF alpha levels were significantly elevated beginning 11 days post infection and increasing levels were measured through day 21. The highest TNF alpha levels in FCL-infected mice were as much as 100-fold higher than in LPS treated non-infected mice. Peak plasma levels of TNF alpha were seen between 1 and 2 hr after LPS induction, as compared to a peak at 1 hr in controls. The ability of LPS to stimulate TNF alpha was concentration dependent over a range of 0.005 to 50 micrograms per mouse. Using anti-TNF alpha antiserum, cytotoxic activity of plasma was shown to be due specifically to TNF alpha. These data suggest that induction of TNF alpha and IL-6 is regulated by different mechanisms in FLC-infected mice.
Friend白血病病毒复合体（FLC）感染BALB/c小鼠会导致大多数免疫功能迅速、进行性抑制。在本研究中，FLC感染导致细菌脂多糖（LPS）诱导肿瘤坏死因子α（TNFα）增加，但不影响白细胞介素-6（IL-6）。感染后11天开始，TNFα水平显著升高，并持续测量至第21天。FLC感染小鼠中TNFα的最高水平比LPS处理的未感染小鼠高出100倍。LPS诱导后1至2小时出现TNFα血浆峰值，而对照组在1小时出现峰值。在每只小鼠0.005至50微克的范围内，LPS刺激TNFα的能力呈浓度依赖性。使用抗TNFα抗血清表明，血浆的细胞毒性活性特异性地归因于TNFα。这些数据表明，在FLC感染的小鼠中，TNFα和IL-6的诱导受不同机制调节。
