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Role of Mitogen-Activated Proteinkinase Activation in the Production of Inflammatory Mediators: Differences Between Primary Rat Alveolar Macrophages and Macrophage Cell Lines

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  • Personal Author:
  • Description:
    Stimulation of macrophages has been shown to activate all three families of mitogen activated protein kinases (MAPKs). However, variable results are reported in the literature with respect to the particular kinases activated with any given stimulus. In this study, the role of activation of MAPKs was examined in the production of inflammatory mediators by measuring the phosphorylation of the kinases and their ability to phosphorylate specific substrates in rat primary alveolar macrophages, a rat alveolar macrophage cell line (NR8383), and two mouse monocytic cell lines (RAW 264.7 and J774A.1). In the three cell lines examined, all three families of MAPKs were activated upon stimulation with either lipopolysaccharide (LPS) or LPS plus interferon-gamma; in contrast, only ERK1/2 was activated in primary rat alveolar macrophages upon stimulation with LPS. Inhibition of ERK1/2 activation by the MEK inhibitor PD98059 abrogated nitric oxide and tumor necrosis factor-alpha (TNF-alpha) production in primary rat alveolar macrophages, but the p38 inhibitor SB203580 had no effect on the production of these two inflammatory mediators. These observations indicate that MAPK activation is cell specific and explain some of the conflicting results reported in the literature. These studies emphasize the need to exercise caution in extrapolating data from cell lines to primary cells. [Description provided by NIOSH]
  • Subjects:
  • Keywords:
  • ISSN:
    0098-4108
  • Document Type:
    Text
  • Genre:
    Journal Article
  • Place as Subject:
  • CIO:
    National Institute for Occupational Safety and Health (NIOSH)
  • Division:
    HELD - Health Effects Laboratory Division
  • Topic:
    Workplace Safety & Health
  • Location:
    North America
  • Volume:
    65
  • Issue:
    10
  • NIOSHTIC Number:
    nn:20022510
  • Citation:
    J Toxicol Environ Health A 2002 May; 65(10):757-768
  • Contact Point Address:
    Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505, USA
  • Email:
    mir8@cdc.gov
  • Federal Fiscal Year:
    2002
  • Peer Reviewed:
    True
  • Source Full Name:
    Journal of Toxicology and Environmental Health, Part A: Current Issues
  • Collection(s):
  • Main Document Checksum:
    urn:sha-512:a599d3e5b0b1ac71fffd9ca9b59efbf9c1b6ff5d62ebb5b2c90d4580947474906cf599a2384cd14f06bebc3f218181ba40180a290cf2d018e23ebbdfdd66b3e0
  • Download URL:
  • File Type:
    Filetype[PDF - 453.22 KB ]
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