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- W2136397744 abstract "Allergic asthma is a chronic inflammatory disorder of the airway associated with bronchial obstruction, airway hyper-reactivity (AHR), and mucus production. The epithelium may direct and propagate asthmatic-like responses. Central to this theory is the observation that viruses, air pollution, and allergens promote epithelial damage and trigger the generation of IL-25, IL-33, and TSLP via innate pathways such as TLRs and purinergic receptors. Similarly, engineered nanomaterials promote a Th2-associated pathophysiology. In this study, we tested the hypothesis that instillation of multi-walled carbon nanotubes (MWCNT) impair pulmonary function in C57Bl/6 mice due to the development of IL-33-dependent Th2-associated inflammation. MWCNT exposure resulted in elevated levels of IL-33 in the lavage fluid (likely originating from airway epithelial cells), enhanced AHR, eosinophil recruitment, and production of Th2-associated cytokines and chemokines. Moreover, these events were dependent on IL-13 signaling and the IL-33/ST2 axis, but independent of T and B cells. Finally, MWCNT exposure resulted in the recruitment of innate lymphoid cells. Collectively, our data suggest that MWCNT induce epithelial damage that results in release of IL-33, which in turn promotes innate lymphoid cell recruitment and the development of IL-13-dependent inflammatory response." @default.
- W2136397744 created "2016-06-24" @default.
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- W2136397744 date "2012-06-29" @default.
- W2136397744 modified "2023-10-10" @default.
- W2136397744 title "<b>IL-33 mediates multi-walled carbon nanotube (MWCNT)-induced airway hyper-reactivity via the mobilization of innate helper cells in the lung</b>" @default.
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- W2136397744 doi "https://doi.org/10.3109/17435390.2012.702230" @default.
- W2136397744 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4080677" @default.
- W2136397744 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22686327" @default.
- W2136397744 hasPublicationYear "2012" @default.
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