Van Miert A S, Van Duin C T, Wensing T
Department of Veterinary Basic Sciences, Faculty of Veterinary Medicine, Utrecht University, The Netherlands.
J Comp Pathol. 1990 Oct;103(3):289-300. doi: 10.1016/s0021-9975(08)80049-7.
Inflammation or invasion by pathogenic micro-organisms induces systemic changes, collectively known as the acute phase response. Among the varied alterations that together produce this response are fever, hypoferraemia and hypozincaemia. It is likely that these responses are mediated, in part, by production and release of cytokines such as interleukin-1 (Il-1), interferons (IFN-alpha) and tumour necrosis factor (TNF). The present report describes a comparative study in dwarf goats on recombinant human IFN-alpha 2a (0.5 x 10(5) IU per kg intravenously (i.v.) and 0.5 x 10(6) IU per kg intramuscularly (i.m.], Poly I:Poly C (an interferon inducer; 30 micrograms per kg i.v.), Newcastle disease virus La Sota strain (an interferon inducer; 0.5 ml per kg i.v.) and Escherichia coli endotoxin (an Il-1 and TNF inducer; 0.1 microgram per kg i.v.). The i.v. injection of recombinant IFN-alpha 2a caused characteristic monophasic febrile reactions, but no significant changes in plasma zinc and iron concentrations. The temperature responses were not due to endotoxin contamination because polymyxin B, which blocks endotoxin, had no inhibitory effect on the pyrogenicity of IFN-alpha 2a. In contrast, the IFN-alpha 2a-induced fever was completely prevented by flurbiprofen pretreatment (1 mg per kg i.v.). In contrast to the i.v. administration, i.m. injection of IFN-alpha 2a caused fever, hypoferraemia and hypozincaemia. Similar results were obtained after E. coli endotoxin, NCD La Sota strain and Poly I:Poly C injection. However, the shapes of the temperature curves and the changes in trace metal concentrations were markedly different. These data support the theory that fever and the changes in plasma zinc and iron concentrations are regulated by different mechanisms.
炎症或病原微生物的侵袭会引发全身性变化，统称为急性期反应。共同产生这种反应的各种变化包括发热、低铁血症和低锌血症。这些反应可能部分是由细胞因子如白细胞介素 -1（Il -1）、干扰素（IFN -α）和肿瘤坏死因子（TNF）的产生和释放介导的。本报告描述了在矮山羊身上进行的一项比较研究，涉及重组人IFN -α 2a（静脉注射每千克0.5×10⁵国际单位和肌肉注射每千克0.5×10⁶国际单位）、聚肌苷酸:聚胞苷酸（一种干扰素诱导剂；静脉注射每千克30微克）、新城疫病毒La Sota株（一种干扰素诱导剂；静脉注射每千克0.5毫升）和大肠杆菌内毒素（一种Il -1和TNF诱导剂；静脉注射每千克0.1微克）。静脉注射重组IFN -α 2a会引起典型的单相发热反应，但血浆锌和铁浓度无显著变化。温度反应并非由内毒素污染引起，因为阻断内毒素的多粘菌素B对IFN -α 2a的致热作用没有抑制作用。相比之下，氟比洛芬预处理（静脉注射每千克1毫克）可完全预防IFN -α 2a诱导的发热。与静脉给药不同，肌肉注射IFN -α 2a会引起发热、低铁血症和低锌血症。注射大肠杆菌内毒素、新城疫病毒La Sota株和聚肌苷酸:聚胞苷酸后也得到了类似结果。然而，温度曲线的形状和微量金属浓度的变化明显不同。这些数据支持了发热以及血浆锌和铁浓度变化由不同机制调节的理论。
