Yanagawa H, Sone S, Haku T, Mizuno K, Yano S, Ohmoto Y, Ogura T
Third Department of Internal Medicine, University of Tokushima School of Medicine, Japan.
Am J Respir Cell Mol Biol. 1995 Jan;12(1):71-6. doi: 10.1165/ajrcmb.12.1.7811472.
We investigated the effect of interleukin-13 (IL-13) on production of IL-1 receptor antagonist (IL-1ra) and proinflammatory cytokines by human alveolar macrophages (AM). AM were obtained by bronchoalveolar lavage from healthy donors. The production of IL-1ra and proinflammatory cytokines, such as IL-1 beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha), were quantitated by enzyme immunoassays. AM spontaneously produced IL-1ra, and this production was significantly augmented by IL-13. On the other hand, IL-13 alone did not affect production of proinflammatory cytokines by freshly isolated AM. Upon stimulation with lipopolysaccharide (LPS), AM produced a significantly amount of proinflammatory cytokines as well as IL-1ra, but this production was suppressed by IL-13 in a dose-dependent manner. In contrast, IL-13 caused a small but reproducible increase in LPS-induced IL-1ra production. These regulatory effects of IL-13 were also observed in blood monocytes and macrophages generated in vitro by maturation of blood monocytes with granulocyte/macrophage colony-stimulating factor. These observations suggest that IL-13 may act as an anti-inflammatory cytokine through regulation of cytokine production by AM in the lung.
我们研究了白细胞介素-13（IL-13）对人肺泡巨噬细胞（AM）产生IL-1受体拮抗剂（IL-1ra）和促炎细胞因子的影响。通过对健康供体进行支气管肺泡灌洗获取AM。采用酶免疫测定法定量检测IL-1ra和促炎细胞因子（如IL-1β、IL-6和肿瘤坏死因子-α（TNF-α））的产生。AM可自发产生IL-1ra，且IL-13可显著增强这种产生。另一方面，单独的IL-13对新鲜分离的AM产生促炎细胞因子没有影响。在用脂多糖（LPS）刺激后，AM产生大量促炎细胞因子以及IL-1ra，但这种产生受到IL-13的剂量依赖性抑制。相反，IL-13使LPS诱导的IL-1ra产生有小幅度但可重复的增加。在血液单核细胞以及通过用粒细胞/巨噬细胞集落刺激因子使血液单核细胞成熟而在体外产生的巨噬细胞中也观察到了IL-13的这些调节作用。这些观察结果表明，IL-13可能通过调节肺中AM的细胞因子产生而作为一种抗炎细胞因子发挥作用。
