Burch R M, Connor J R, Tiffany C W
Nova Pharmaceutical Corp., Baltimore, MD 21224.
Agents Actions. 1989 Jun;27(3-4):258-60. doi: 10.1007/BF01972790.
We examined bradykinin's effects on macrophages and fibroblasts, two cell types important in the pathogenesis of chronic inflammation. Bradykinin stimulated release of proteins of 18 kDa from macrophages. These proteins caused increased thymocyte proliferation (interleukin 1, IL-1) and completely inhibited lipoprotein lipase (tumor necrosis factor, TNF). When fibroblasts were incubated with bradykinin, PGE2 synthesis was stimulated. Pretreatment with IL-1 or TNF dramatically amplified bradykinin-stimulated PGE2 synthesis. Thus, bradykinin is involved in a positive feedback loop in which bradykinin activates macrophages to release potent inflammatory cytokines; these in turn amplify responsiveness of bradykinin target tissues.
我们研究了缓激肽对巨噬细胞和成纤维细胞的作用，这两种细胞类型在慢性炎症的发病机制中很重要。缓激肽刺激巨噬细胞释放18 kDa的蛋白质。这些蛋白质导致胸腺细胞增殖增加（白细胞介素1，IL-1）并完全抑制脂蛋白脂肪酶（肿瘤坏死因子，TNF）。当成纤维细胞与缓激肽一起孵育时，PGE2的合成受到刺激。用IL-1或TNF预处理可显著增强缓激肽刺激的PGE2合成。因此，缓激肽参与了一个正反馈回路，其中缓激肽激活巨噬细胞释放强效炎症细胞因子；这些细胞因子反过来又增强了缓激肽靶组织的反应性。
