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.
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