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Abstract

Airway exposure to endotoxin and other microbial TLR agonists induces a rapid production of mediators including IL-1 and IL-17, neutrophil recruitment, and bronchoconstriction which are abrogated in mice deficient for distinct TLRs or the common adaptor molecule myeloid differentiation factor 88 (MyD88). Furthermore, administration of IL-1β mobilizes neutrophils and induces IL-17 production in the lung. Therefore, IL-17 participates in IL-1β-induced lung inflammation. Importantly, lung injury by particles, chemicals, and allergens activates the NLPR3 inflammasome complex leading to the cleavage of pro-IL-1β into active IL-1β- and IL-17-dependent inflammation and repair. In conclusion, TLR agonists and lung injury induces the activation of the NLPR inflammasome with maturation of IL-1β leading to IL-17-dependent lung inflammation.

Grant support by “Ministère de l’Education Nationale, de la Recherche et de la Technologie,” Fondation de la Recherche, and CNRS. The work was also supported by grants from Le Studium (Orleans), Biomedical Research Foundation, and Fondation de la Recherche Médicale.

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Abbreviations

LPS:

Lipopolysaccharide

TLR:

Toll-like receptor

TIR:

Toll-interleukin 1 receptor

TIRAP:

TIR-domain-containing adaptor protein

TRIF:

TIR-domain-containing adaptor-inducing interferon-β

Penh:

Enhanced respiratory pause

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Correspondence to Isabelle Couillin .

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Couillin, I. et al. (2013). Inflammasome: IL-1/IL-17 Response in Lung Inflammation. In: Quesniaux, V., Ryffel, B., Padova, F. (eds) IL-17, IL-22 and Their Producing Cells: Role in Inflammation and Autoimmunity. Progress in Inflammation Research. Springer, Basel. https://doi.org/10.1007/978-3-0348-0522-3_11

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  • DOI: https://doi.org/10.1007/978-3-0348-0522-3_11

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