IL-1β-stimulated activation of ERK1/2 and p38α MAPK mediates the transcriptional up-regulation of IL-6, IL-8 and GRO-α in HeLa cells

Huei-Ting Yang, Philip Cohen, Simon Rousseau

    Research output: Contribution to journalArticlepeer-review

    42 Citations (Scopus)


    Epithelial cells represent the first line of defense against infection. Here we have studied the production of inflammatory mediators induced by IL-1ß in the HeLa epithelial cell line. We found that GRO-a, IL-6 and IL-8 were the only three inflammatory mediators elevated out of 36 tested. Specific inhibition of p38a MAP kinase or preventing the activation of ERK1/ERK2 partially reduced the production of these substances, while the combined blockade of both pathways almost abolished secretion. The suppression of these signaling pathways mainly reduced transcription of the genes encoding GRO-a, IL-6 and IL-8, rather than affecting mRNA stability, translation or secretion. The production of these three inflammatory mediators was shown to account for the ability of the HeLa cell culture medium to stimulate the migration of monocytes/macrophages, suggesting a key role for p38 MAPK and ERK1/ERK2 in orchestrating the epithelial cell response to infection.
    Original languageEnglish
    Pages (from-to)375-380
    Number of pages6
    JournalCellular Signalling
    Issue number2
    Publication statusPublished - Feb 2008


    • Cell Movement
    • Chemokine CXCL1
    • Cytokines
    • Enzyme Activation
    • HeLa Cells
    • Humans
    • Interleukin-1beta
    • Interleukin-6
    • Interleukin-8
    • MAP Kinase Signaling System
    • Macrophages
    • Mitogen-Activated Protein Kinase 1
    • Mitogen-Activated Protein Kinase 3
    • Monocytes
    • Receptors, Interleukin-1
    • Transcription, Genetic
    • Up-Regulation
    • p38 Mitogen-Activated Protein Kinases

    Cite this