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Contribution of IL-17 to the pulmonary inflammatory response

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Th 17 Cells: Role in Inflammation and Autoimmune Disease

Abstract

Airway exposure to endotoxin and other microbial Toll-like receptor (TLR) agonists induces a rapid production of mediators including IL-1, neutrophil recruitment and bronchoconstriction, which are abrogated in mice deficient for distinct TLRs or the common adaptor molecule myeloid differentiation factor 88 (MyD88). Intranasal IL-17 administration causes acute neutrophilic lung inflammation in a proinflammatory environment. Recent investigations revealed that IL-17 is up-regulated upon endotoxin aerosol exposure and neutralization of IL-17 diminished endotoxininduced inflammation, suggesting a role of endogenous IL-17 in endotoxin-induced lung inflammation. Furthermore, administration of IL-1β mobilizes neutrophils and induces IL-17 production in the lung. Therefore, IL-17 might participates in IL-1β-induced lung inflammation. Importantly, lung injury leads to NALP3 inflammasome activation, leading to IL-1β-dependent acute inflammation. The participation of IL-17 in this response is discussed. In conclusion, TLR-agonist and injury-induced lung inflammation depend in part on IL-1β and IL-17. The role of inflammasome activation cleaving pro-IL-1β leading to mature IL-1ß and IL-1β-dependent IL-17 production and inflammation need to be explored further.

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Couillin, I. et al. (2009). Contribution of IL-17 to the pulmonary inflammatory response. In: Quesniaux, V., Ryffel, B., Di Padova, F. (eds) Th 17 Cells: Role in Inflammation and Autoimmune Disease. Progress in Inflammation Research. Birkhäuser Basel. https://doi.org/10.1007/978-3-7643-8681-8_9

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  • DOI: https://doi.org/10.1007/978-3-7643-8681-8_9

  • Publisher Name: Birkhäuser Basel

  • Print ISBN: 978-3-7643-8680-1

  • Online ISBN: 978-3-7643-8681-8

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