کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5562587 | 1562702 | 2017 | 11 صفحه PDF | دانلود رایگان |
- Different types of dung smoke increase IL-8, GM-CSF, and Cox-2 in SAECs.
- AhR and AP-1 are activated by dung smoke from different species.
- Dung smoke suppresses the expression of IFNs and IP-10 after a viral-like challenge.
- Supports epidemiological data that dung smoke increases the risk of lung diseases
Worldwide, over 4 million premature deaths each year are attributed to the burning of biomass fuels for cooking and heating. Epidemiological studies associate household air pollution with lung diseases, including chronic obstructive pulmonary disease, lung cancer, and respiratory infections. Animal dung, a biomass fuel used by economically vulnerable populations, generates more toxic compounds per mass burned than other biomass fuels. The type of animal dung used varies widely depending on local agro-geography. There are currently neither standardized experimental systems for dung biomass smoke research nor studies assessing the health impacts of different types of dung smoke. Here, we used a novel reproducible exposure system to assess outcomes related to inflammation and respiratory infections in human airway cells exposed to six different types of dung biomass smoke. We report that dung biomass smoke, regardless of species, is pro-inflammatory and activates the aryl hydrocarbon receptor and JNK transcription factors; however, dung smoke also suppresses interferon responses after a challenge with a viral mimetic. These effects are consistent with epidemiological data, and suggest a mechanism by which the combustion of animal dung can directly cause lung diseases, promote increased susceptibility to infection, and contribute to the global health problem of household air pollution.
166
Journal: Toxicology in Vitro - Volume 43, September 2017, Pages 76-86