Shalit F, Sredni B, Rosenblatt-Bin H, Kazimirsky G, Brodie C, Huberman M
C.A.I.R. Institute, The Marilyn Finkler Cancer Research Center, Bar Ilan University, Ramat Gan, Israel.
Neuroreport. 1997 Nov 10;8(16):3577-80. doi: 10.1097/00001756-199711100-00031.
We investigated the effect of beta-amyloid peptide (betaA) on the activation of the murine-derived monocyte/macrophage J774 cell-line. BetaA induced tumor necrotic factor-alpha (TNF alpha) in these cells in a dose-dependent manner. Incubation of cells with betaA slightly increased nitric oxide (NO) production, an effect that was significantly enhanced by the addition of interferon-gamma (IFN gamma). Substitution of betaA4 with TFN alpha and incubation of the cultures with IFN gamma resulted in significant NO production, although this was lower than that obtained in the presence of the peptide. Incubation of cultures with a monoclonal antibody (mAb) against TNF alpha abrogated NO production. Our results suggest that betaA4-induced TNF alpha production is a crucial event in the activation of peripheral macrophages.
我们研究了β-淀粉样肽(βA)对源自小鼠的单核细胞/巨噬细胞J774细胞系激活的影响。βA以剂量依赖的方式诱导这些细胞产生肿瘤坏死因子-α(TNFα)。用βA孵育细胞会轻微增加一氧化氮(NO)的产生,添加干扰素-γ(IFNγ)可显著增强这种作用。用TNFα替代βA4并与IFNγ一起孵育培养物会导致显著的NO产生,尽管这低于在肽存在时获得的产量。用抗TNFα单克隆抗体(mAb)孵育培养物可消除NO的产生。我们的结果表明,βA4诱导的TNFα产生是外周巨噬细胞激活中的关键事件。