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    IL-1b and TNF-a induce increased expression of CCL28 by airway epithelial cells via an NFjB-dependent pathway

    O'Gorman, Mary T. and Jatoi, Noor A. and Lane, Stephen J. and Mahon, Bernard P. (2005) IL-1b and TNF-a induce increased expression of CCL28 by airway epithelial cells via an NFjB-dependent pathway. Cellular Immunology, 238. pp. 87-96.

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    CCL28 is a mucosal chemokine that attracts eosinophils and T cells via the receptors CCR3 and CCR10. Consequently, it is a candidate mediator of the pathology associated with asthma. This study examined constitutive and induced expression of CCL28 by A549 human airway epithelial-like cells. Real-time RT-PCR and ELISA of cultured cells and supernatants revealed constitutive levels of CCL28 expression to be low, whereas IL-1b and TNF-a, induced significantly increased expression. Observations from induced sputum and human airway biopsies supported this. Signal transduction studies revealed that IL-1b and TNF-a stimulation induced NFjB phosphorylation in A549 cells, but antagonist inhibition of NFjB p50–p65 phosphorylation correlated with marked reduction of IL-1b or TNF-a induced CCL28 expression. Together these studies imply a role for CCL28 in the orchestration of airway inflammation, and suggest that CCL28 is one link between microbial insult and the exacerbation of pathologies such as asthma, through an NFjB-dependent mechanism.

    Item Type: Article
    Keywords: CCL28; IL-1b; TNF-a; Respiratory tract; NFjB; Asthma;
    Academic Unit: Faculty of Science and Engineering > Biology
    Faculty of Science and Engineering > Research Institutes > Institute of Immunology
    Item ID: 511
    Depositing User: Bernard Mahon
    Date Deposited: 23 Sep 2008
    Journal or Publication Title: Cellular Immunology
    Publisher: Elsevier
    Refereed: Yes
    Use Licence: This item is available under a Creative Commons Attribution Non Commercial Share Alike Licence (CC BY-NC-SA). Details of this licence are available here

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