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© Research
Publication : PloS one

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

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in PloS one - 16 Aug 2011

Gasse P, Riteau N, Vacher R, Michel ML, Fautrel A, di Padova F, Fick L, Charron S, Lagente V, Eberl G, Le Bert M, Quesniaux VF, Huaux F, Leite-de-Moraes M, Ryffel B, Couillin I

Link to Pubmed [PMID] – 21858022

PLoS ONE 2011;6(8):e23185

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.

http://www.ncbi.nlm.nih.gov/pubmed/21858022