| Autor: |
Beamer CA; Department of Biomedical and Pharmaceutical Sciences, Center for Environmental Health Sciences, The University of Montana, Missoula, MT 59812-1552, USA. celine.beamer@umontana.edu, Girtsman TA, Seaver BP, Finsaas KJ, Migliaccio CT, Perry VK, Rottman JB, Smith DE, Holian A |
| Jazyk: |
angličtina |
| Zdroj: |
Nanotoxicology [Nanotoxicology] 2013 Sep; Vol. 7 (6), pp. 1070-81. Date of Electronic Publication: 2012 Jun 29. |
| DOI: |
10.3109/17435390.2012.702230 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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