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首页> 美国卫生研究院文献>The Journal of Experimental Medicine >Production of Mice Deficient in Genes for Interleukin (IL)-1α IL-1β IL-1α/β and IL-1 Receptor Antagonist Shows that IL-1β Is Crucial in Turpentine-induced Fever Development and Glucocorticoid Secretion
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Production of Mice Deficient in Genes for Interleukin (IL)-1α IL-1β IL-1α/β and IL-1 Receptor Antagonist Shows that IL-1β Is Crucial in Turpentine-induced Fever Development and Glucocorticoid Secretion

机译：缺乏白介素（IL）-1αIL-1βIL-1α/β和IL-1受体拮抗剂基因的小鼠的产生表明IL-1β在松节油诱导的发热发展和糖皮质激素分泌中至关重要

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Interleukin (IL)-1 is a major mediator of inflammation and exerts pleiotropic effects on the neuro-immuno-endocrine system. To elucidate pathophysiological roles of IL-1, we have first produced IL-1α/β doubly deficient (KO) mice together with mice deficient in either the IL-1α, IL-1β, or IL-1 receptor antagonist (IL-1ra) genes. These mice were born healthy, and their growth was normal except for IL-1ra KO mice, which showed growth retardation after weaning. Fever development upon injection with turpentine was suppressed in IL-1β as well as IL-1α/β KO mice, but not in IL-1α KO mice, whereas IL-1ra KO mice showed an elevated response. At this time, expression of IL-1β mRNA in the diencephalon decreased 1.5-fold in IL-1α KO mice, whereas expression of IL-1α mRNA decreased >30-fold in IL-1β KO mice, suggesting mutual induction between IL-1α and IL-1β. This mutual induction was also suggested in peritoneal macrophages stimulated with lipopolysaccharide in vitro. In IL-1β KO mice treated with turpentine, the induction of cyclooxygenase-2 (EC 1.14.99.1) in the diencephalon was suppressed, whereas it was enhanced in IL-1ra KO mice. We also found that glucocorticoid induction 8 h after turpentine treatment was suppressed in IL-1β but not IL-1α KO mice. These observations suggest that IL-1β but not IL-1α is crucial in febrile and neuro-immuno-endocrine responses, and that this is because IL-1α expression in the brain is dependent on IL-1β. The importance of IL-1ra both in normal physiology and under stress is also suggested.
机译：白介素（IL）-1是炎症的主要介质，对神经免疫-内分泌系统起多效作用。为了阐明IL-1的病理生理作用，我们首先生产了IL-1α/β双倍缺乏（KO）小鼠以及缺乏IL-1α，IL-1β或IL-1受体拮抗剂（IL-1ra）的小鼠基因。这些小鼠天生健康，除IL-1ra KO小鼠外，其生长正常，IL-1ra KO小鼠在断奶后表现出生长迟缓。 IL-1β和IL-1α/βKO小鼠抑制了注射松节油后的发热，但IL-1αKO小鼠没有抑制，而IL-1ra KO小鼠显示升高的反应。此时，IL-1αKO小鼠的间脑中IL-1βmRNA的表达降低了1.5倍，而IL-1βKO小鼠的IL-1αmRNA的表达降低了> 30倍，表明IL-1α之间的相互诱导和IL-1β。在体外用脂多糖刺激的腹膜巨噬细胞中也提示了这种相互诱导。在用松节油处理过的IL-1βKO小鼠中，间脑中环氧合酶2（EC 1.14.99.1）的诱导被抑制，而在IL-1ra KO小鼠中则增强了。我们还发现，IL-1β抑制了松节油处理后8 h的糖皮质激素诱导，而IL-1αKO小鼠则没有。这些观察结果表明，IL-1β对发热和神经免疫内分泌反应至关重要，这是因为脑中IL-1α的表达依赖于IL-1β。还建议了IL-1ra在正常生理和压力下的重要性。

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