Neuroimmunologyβ-Amyloid peptide induces tumor necrosis factor-α and nitric oxide production in murine macrophage culturesShalit, Frances1; Sredni, Benjamin1,4; Rosenblatt-Bin, Hannah1; Kazimirsky, Gila2; Brodie, Chaya2; Huberman, Moshe3Author Information 1C.A.I.R. Institute, The Marilyn Finkler Cancer Research Center, Bar Ilan University, Ramat Gan, 52900 Israel 2Department of Life Sciences, Bar Ilan University, Ramat Gan, 52900 Israel 3Department of Neurology, Meir Hospital, Kfar Saba, Israel, Sackler School of Medicine, Tel Aviv University, Israel 4Corresponding Author: Benjamin Sredni Received 6 August 1997; accepted 7 September 1997 NeuroReport: November 10th, 1997 - Volume 8 - Issue 16 - p 3577-3580 Buy Abstract We investigated the effect of β-amyloid peptide (βA) on the activation of the murine-derived monocyte/macrophage J774 cell-line. βA induced tumor necrotic factor-α(TNFα) in these cells in a dose-dependent manner. Incubation of cells with βA slightly increased nitric oxide (NO) production, an effect that was significantly enhanced by the addition of interferon-γ(IFNγ). Substitution of βA4 with TFNα and incubation of the cultures with IFNγ 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 TNFα abrogated NO production. Our results suggest that βA4-induced TNFα production is a crucial event in the activation of peripheral macrophages. © Lippincott-Raven Publishers.