Pettipher E R, Higgs G A, Henderson B
Proc Natl Acad Sci U S A. 1986 Nov;83(22):8749-53. doi: 10.1073/pnas.83.22.8749.
Interleukin 1 (IL-1) is a polypeptide released by activated macrophages and is thought to be a key mediator of host responses to infection and inflammation. The availability of highly purified and recombinant material has now permitted the evaluation of IL-1 as a mediator of chronic inflammatory processes in vivo. We have demonstrated that intraarticular injection of IL-1 into rabbit knee joints induces the accumulation of polymorphonuclear and mononuclear leukocytes in the joint space and the loss of proteoglycan from the articular cartilage. The effects on cartilage could not be explained solely by the presence of leukocytes, since injections of endotoxin also stimulated leukocyte accumulation in the joint but had no effect on proteoglycan loss. Responses to IL-1 were not associated with increased production of the icosanoids prostaglandin E2 or leukotriene B4 and were not reduced by an inhibitor of their synthesis. The pattern of leukocyte infiltration and cartilage breakdown 24 hr after IL-1 injection was similar to that seen in animals with antigen-induced arthritis of 1 week's duration. These observations support the hypothesis that IL-1 acts directly to mediate the erosive processes of chronic arthritis.
白细胞介素1（IL-1）是一种由活化巨噬细胞释放的多肽，被认为是宿主对感染和炎症反应的关键介质。现在，高纯度和重组材料的可得性使得人们能够在体内评估IL-1作为慢性炎症过程介质的作用。我们已经证明，向兔膝关节内注射IL-1会导致关节腔内多形核白细胞和单核白细胞的积聚以及关节软骨中蛋白聚糖的丢失。对软骨的影响不能仅由白细胞的存在来解释，因为注射内毒素也会刺激关节内白细胞的积聚，但对蛋白聚糖的丢失没有影响。对IL-1的反应与类二十烷酸前列腺素E2或白三烯B4的产生增加无关，并且其合成抑制剂也不能使其反应减弱。注射IL-1后24小时白细胞浸润和软骨破坏的模式与患有持续1周的抗原诱导性关节炎的动物相似。这些观察结果支持了IL-1直接介导慢性关节炎侵蚀过程的假说。
