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    Myeloid-derived miR-223 regulates intestinal inflammation via repression of the NLRP3 inflammasome

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    Author
    Neudecker, V; Haneklaus, M; Jensen, O; Khailova, L; Masterson, JC; Tye, H; Biette, K; Jedlicka, P; Brodsky, KS; Gerich, ME; ...
    Date
    2017-06-01
    Source Title
    Journal of Experimental Medicine
    Publisher
    ROCKEFELLER UNIV PRESS
    University of Melbourne Author/s
    Masters, Seth
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Neudecker, V., Haneklaus, M., Jensen, O., Khailova, L., Masterson, J. C., Tye, H., Biette, K., Jedlicka, P., Brodsky, K. S., Gerich, M. E., Mack, M., Robertson, A. A. B., Cooper, M. A., Furuta, G. T., Dinarello, C. A., O'Neill, L. A., Eltzschig, H. K., Masters, S. L. & McNamee, E. N. (2017). Myeloid-derived miR-223 regulates intestinal inflammation via repression of the NLRP3 inflammasome. JOURNAL OF EXPERIMENTAL MEDICINE, 214 (6), pp.1737-1752. https://doi.org/10.1084/jem.20160462.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/254627
    DOI
    10.1084/jem.20160462
    Abstract
    MicroRNA (miRNA)-mediated RNA interference regulates many immune processes, but how miRNA circuits orchestrate aberrant intestinal inflammation during inflammatory bowel disease (IBD) is poorly defined. Here, we report that miR-223 limits intestinal inflammation by constraining the nlrp3 inflammasome. miR-223 was increased in intestinal biopsies from patients with active IBD and in preclinical models of intestinal inflammation. miR-223-/y mice presented with exacerbated myeloid-driven experimental colitis with heightened clinical, histopathological, and cytokine readouts. Mechanistically, enhanced NLRP3 inflammasome expression with elevated IL-1β was a predominant feature during the initiation of colitis with miR-223 deficiency. Depletion of CCR2+ inflammatory monocytes and pharmacologic blockade of IL-1β or NLRP3 abrogated this phenotype. Generation of a novel mouse line, with deletion of the miR-223 binding site in the NLRP3 3' untranslated region, phenocopied the characteristics of miR-223-/y mice. Finally, nanoparticle-mediated overexpression of miR-223 attenuated experimental colitis, NLRP3 levels, and IL-1β release. Collectively, our data reveal a previously unappreciated role for miR-223 in regulating the innate immune response during intestinal inflammation.

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