title: Pro-inflammatory effects of aluminum in human glioblastoma cells.
abstract: Inflammatory events have been associated with senile plaques, one of the pathological hallmarks of Alzheimer's disease (AD). It is believed that aggregated beta-amyloid (betaA) proteins, which form the core of these plaques, may be responsible for triggering the inflammatory reaction. In the present study, the ability of aluminum (Al) to initiate similar inflammatory events was investigated in a human glioblastoma cell line. A 6-day exposure to either lipopolysaccharide (LPS) or aluminum sulfate caused a significant increase in the rate of proliferation of the glioblastoma cells. Both treatments also caused activation of the immune-responsive transcription factor NF-kappaB although there were time-related differences. The levels of secreted cytokines, interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) were both increased by the LPS treatment although exposure to Al decreased the secretion of the former while elevating the levels of the latter. These events may be due to the activation of glial cells and subsequent stress response to either Al complexes or LPS. Although exposure to either stress factor caused a stimulation of inflammatory markers, there were time-dependent differences in the response. This may reflect the ability of the cells to discern different stress factors and thus orchestrate an innate immune response profile distinct to each immunogen.
authors.affiliation: Department of Community and Environmental Medicine, Center for Occupational and Environmental Health, University of California-Irvine, Irvine, CA 92697-1820, USA. aghadimi@uci.edu
authors.forename: Arezoo
authors.initials: A
authors.lastname: Campbell
authors.forename: Ellen Y
authors.initials: EY
authors.lastname: Yang
authors.forename: Mindy
authors.initials: M
authors.lastname: Tsai-Turton
authors.forename: Stephen C
authors.initials: SC
authors.lastname: Bondy
mesh_terms: D000534:Alum Compounds / Q000009:adverse effects*; D002455:Cell Division / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D005909:Glioblastoma; D006801:Humans; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism; D018836:Inflammation Mediators / Q000009:adverse effects*; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides; D016328:NF-kappa B / Q000378:metabolism; D009457:Neuroglia / Q000187:drug effects* / Q000378:metabolism; D013997:Time Factors; D014407:Tumor Cells, Cultured; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000534:Alum Compounds; D018836:Inflammation Mediators; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; C041524:aluminum sulfate