IL-12 attenuates bleomycin-induced pulmonary fibrosis
IL-12 attenuates bleomycin-induced pulmonary fibrosis
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DOI：
10.1152/ajplung.2001.281.1.l92
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发表时间：
2001-07-01
影响因子：
4.9
通讯作者：
Strieter, RM
中科院分区：
文献类型：
--
作者：
Keane, MP;Belperio, JA;Strieter, RM
白细胞介素(IL)-12是干扰素(IFN)- γ的有效诱导剂。我们假设IL-12可以减轻博莱霉素诱导的肺纤维化。为了验证这一假设，我们每天给博莱霉素治疗的小鼠腹腔注射IL-12或小鼠血清白蛋白，直到第12天。与对照组相比，经IL-12处理的小鼠羟脯氨酸水平降低。此外，给药IL-12导致肺和支气管肺泡灌洗液ifn - γ的时间依赖性增加。同时给予中和性抗ifn - γ抗体可减弱IL-12的抗纤维化作用。这些发现支持了IL-12通过调节ifn - γ的产生来减弱博莱霉素诱导的肺纤维化的观点。
Interleukin (IL)-12 is a potent inducer of interferon (IFN)-gamma. We postulated that IL-12 would attenuate bleomycin-induced pulmonary fibrosis. To test this hypothesis, we administered IL-12 or murine serum albumin to bleomycin-treated mice by daily intraperitoneal injection until day 12. Mice treated with IL-12 demonstrated decreased hydroxyproline levels compared with control treated mice. Furthermore, administration of IL-12 led to a time-dependent increase in both lung and bronchoalveolar lavage fluid IFN-gamma. The antifibrotic effect of IL-12 could be attenuated with simultaneous administration of neutralizing anti-IFN-gamma antibodies. These findings support the notion that IL-12 attenuates bleomycin-induced pulmonary fibrosis via modulation of IFN-gamma production.