IL-1 and IL-23 mediate early IL-17A production in pulmonary inflammation leading to late fibrosis

 

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dc.contributor.author Gasse, Paméla en_ZA
dc.contributor.author Riteau, Nicolas en_ZA
dc.contributor.author Vacher, Rachel en_ZA
dc.contributor.author Michel, Marie-Laure en_ZA
dc.contributor.author Fautrel, Alain en_ZA
dc.contributor.author di Padova, Franco en_ZA
dc.contributor.author Fick, Lizette en_ZA
dc.contributor.author Charron, Sabine en_ZA
dc.contributor.author Lagente, Vincent en_ZA
dc.contributor.author Eberl, Gérard en_ZA
dc.date.accessioned 2016-01-02T05:05:49Z
dc.date.available 2016-01-02T05:05:49Z
dc.date.issued 2011 en_ZA
dc.identifier.citation Gasse, P., Riteau, N., Vacher, R., Michel, M. L., Fautrel, A., Di Padova, F., ... & Le Bert, M. (2011). IL-1 and IL-23 mediate early IL-17A production in pulmonary inflammation leading to late fibrosis. PloS one, 6(8), e23185. doi:10.1371/journal.pone.0023185 en_ZA
dc.identifier.uri http://hdl.handle.net/11427/16164
dc.identifier.uri http://dx.doi.org/10.1371/journal.pone.0023185
dc.description.abstract BACKGROUND: Idiopathic pulmonary fibrosis is a devastating as yet untreatable disease. We demonstrated recently the predominant role of the NLRP3 inflammasome activation and IL-1β expression in the establishment of pulmonary inflammation and fibrosis in mice. METHODS: The contribution of IL-23 or IL-17 in pulmonary inflammation and fibrosis was assessed using the bleomycin model in deficient mice. RESULTS: We show that bleomycin or IL-1β-induced lung injury leads to increased expression of early IL-23p19, and IL-17A or IL-17F expression. Early IL-23p19 and IL-17A, but not IL-17F, and IL-17RA signaling are required for inflammatory response to BLM as shown with gene deficient mice or mice treated with neutralizing antibodies. Using FACS analysis, we show a very early IL-17A and IL-17F expression by RORγt + γδ T cells and to a lesser extent by CD4αβ + T cells, but not by iNKT cells, 24 hrs after BLM administration. Moreover, IL-23p19 and IL-17A expressions or IL-17RA signaling are necessary to pulmonary TGF-β1 production, collagen deposition and evolution to fibrosis. CONCLUSIONS: Our findings demonstrate the existence of an early IL-1β-IL-23-IL-17A axis leading to pulmonary inflammation and fibrosis and identify innate IL-23 and IL-17A as interesting drug targets for IL-1β driven lung pathology. en_ZA
dc.language.iso eng en_ZA
dc.publisher Public Library of Science en_ZA
dc.rights This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. en_ZA
dc.rights.uri http://creativecommons.org/licenses/by/4.0 en_ZA
dc.source PLoS One en_ZA
dc.source.uri http://journals.plos.org/plosone en_ZA
dc.subject.other T cells en_ZA
dc.subject.other Inflammation en_ZA
dc.subject.other Fibrosis en_ZA
dc.subject.other Collagens en_ZA
dc.subject.other Enzyme-linked immunoassays en_ZA
dc.subject.other Neutrophils en_ZA
dc.subject.other Pulmonary fibrosis en_ZA
dc.subject.other Inflammatory diseases en_ZA
dc.title IL-1 and IL-23 mediate early IL-17A production in pulmonary inflammation leading to late fibrosis en_ZA
dc.type Journal Article en_ZA
dc.rights.holder © 2011 Gasse et al en_ZA
uct.type.publication Research en_ZA
uct.type.resource Article en_ZA
dc.publisher.institution University of Cape Town
dc.publisher.faculty Faculty of Health Sciences en_ZA
dc.publisher.department Institute of Infectious Disease and Molecular Medicine en_ZA
uct.type.filetype Text
uct.type.filetype Image


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This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Except where otherwise noted, this item's license is described as This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.