Cartmell T, Ball C, Bristow A F, Mitchell D, Poole S
National Institute for Biological Standards and Control, Blanche Lane, South Mimms, Potters Bar, Hertfordshire EN6 3QG, UK.
J Physiol. 2003 Jun 1;549(Pt 2):653-64. doi: 10.1113/jphysiol.2002.037291. Epub 2003 Apr 11.
We tested the hypothesis that endogenous interleukin (IL)-10 limits the fever induced by a Gram-negative bacterial toxin (Escherichia coli lipopolysaccharide, LPS) and a Gram-positive bacterial toxin (Staphylococcus aureus), when these toxins are injected into a subcutaneous air pouch (I.PO.) in rats. Injection of LPS or S. aureus caused fevers that were reduced in amplitude and duration by simultaneous administration of rat recombinant IL-10. The inhibition of fever by IL-10 was accompanied by a significant reduction in the toxin-evoked increases in concentrations of immunoreactive IL-6 at the site of inflammation and of IL-6 and IL-1 receptor antagonist in the circulation. Conversely, neutralisation of endogenous IL-10 in the pouch increased the amplitude and dramatically increased the duration of toxin-evoked fever, and augmented toxin-induced increases in pouch tumour necrosis factor-alpha, IL-1beta, and especially IL-6. Our data support a crucial regulatory role for endogenous IL-10 in limiting the fever responses during both Gram-negative and Gram-positive infections.
当将革兰氏阴性菌毒素（大肠杆菌脂多糖，LPS）和革兰氏阳性菌毒素（金黄色葡萄球菌）注射到大鼠的皮下气囊（I.PO.）中时，内源性白细胞介素（IL）-10会限制由这些毒素诱导的发热。注射LPS或金黄色葡萄球菌会引起发热，同时给予大鼠重组IL-10可使发热的幅度和持续时间降低。IL-10对发热的抑制作用伴随着炎症部位免疫反应性IL-6浓度以及循环中IL-6和IL-1受体拮抗剂的毒素诱发增加的显著降低。相反，气囊中内源性IL-10的中和增加了毒素诱发发热的幅度，并显著延长了其持续时间，同时增强了毒素诱导的气囊肿瘤坏死因子-α、IL-1β尤其是IL-6的增加。我们的数据支持内源性IL-10在限制革兰氏阴性和革兰氏阳性感染期间的发热反应中起关键调节作用。
