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  • Mechanisms of interleukin-25 (IL-17E)-induced pulmonary inflammation and airways hyper-reactivity

    Author(s)
    Sharkhuu, T.
    Matthaei, K.
    Forbes, E.
    Mahalingam, S.
    Hogan, S.
    Hansbro, P.
    Foster, P.
    Griffith University Author(s)
    Mahalingam, Suresh
    Year published
    2006
    Metadata
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    Abstract
    Background IL-25, a novel member of the IL-17 cytokine family, promotes CD4+ T-helper 2 lymphocyte-like (Th type-2) inflammatory responses in the lung. Although IL-25 up-regulates IL-13 in the lung, the contribution of this and other type 2 cytokine signalling pathways to the induction and persistence of airways hyper-reactivity (AHR) and allergic inflammation are unclear. Objective To determine the downstream factors employed by IL-25 to induce Th type-2 pulmonary inflammation and AHR. Methods IL-25 was delivered to the airways of BALB/c mice by intra-tracheal (i.t.) instillation and AHR and Th type-2 inflammatory ...
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    Background IL-25, a novel member of the IL-17 cytokine family, promotes CD4+ T-helper 2 lymphocyte-like (Th type-2) inflammatory responses in the lung. Although IL-25 up-regulates IL-13 in the lung, the contribution of this and other type 2 cytokine signalling pathways to the induction and persistence of airways hyper-reactivity (AHR) and allergic inflammation are unclear. Objective To determine the downstream factors employed by IL-25 to induce Th type-2 pulmonary inflammation and AHR. Methods IL-25 was delivered to the airways of BALB/c mice by intra-tracheal (i.t.) instillation and AHR and Th type-2 inflammatory responses were characterized in wild type (WT) and Th type-2-cytokine and -signalling pathway-deficient (-/-) mice. Results IL-25 treatment resulted in AHR, eosinophilic inflammation, mucus hypersecretion and a progressive increase in the production of Th type-2 cytokines in the lungs. Levels of arginase-I (arg-I) and eotaxin were also elevated by IL-25 treatment. A significant reduction in AHR, and attenuation of mucus production was observed in IL-25-treated IL-13-/-, IL-4 receptor alpha (IL-4Ra-/-)- and signal-transducer-and-activator-of-transcription-factor-6 (STAT6-/-)-deficient mice. AHR was also inhibited in IL-4-/-- and IL-5/eotaxin(1)-/-- deficient mice treated with IL-25, however, mucus hypersecretion was not completely ablated. IL-25 promoted Th type-2 responses by directly acting on naﶥ T cells. Conclusion IL-25 potently (single dose) induces sustained AHR and acute pulmonary inflammation with eosinophilia. IL-25-induced AHR is dependent on the production of Th type-2 cytokines, and removal of IL-13 and its signal transduction pathway prevents IL-25-induced airways inflammation and AHR. IL-25 potently induces inflammatory cascades that may exacerbate allergic airways inflammation by promoting Th type-2 cytokine responses in conjunction with the up-regulation of factors (eotaxin and arg-I) that can amplify inflammation associated with allergic disorders. Dysregulation in IL-25 production may predispose to features of allergic airways disease.
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    Journal Title
    Clinical and Experimental Allergy
    Volume
    36
    Issue
    12
    DOI
    https://doi.org/10.1111/j.1365-2222.2006.02595.x
    Subject
    Immunology not elsewhere classified
    Immunology
    Nutrition and Dietetics
    Public Health and Health Services
    Publication URI
    http://hdl.handle.net/10072/55132
    Collection
    • Journal articles

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