Version 1
: Received: 13 August 2020 / Approved: 14 August 2020 / Online: 14 August 2020 (09:22:59 CEST)
How to cite:
zhang, C.; Asif, H.; Calcagno, T. M.; Kumar, N.; Fregien, N. L.; Mirsaeidi, M. Indoor PM10 Upregulates Pro-inflammatory Mediators in Bronchial Epithelial Cells. Preprints2020, 2020080315. https://doi.org/10.20944/preprints202008.0315.v1
zhang, C.; Asif, H.; Calcagno, T. M.; Kumar, N.; Fregien, N. L.; Mirsaeidi, M. Indoor PM10 Upregulates Pro-inflammatory Mediators in Bronchial Epithelial Cells. Preprints 2020, 2020080315. https://doi.org/10.20944/preprints202008.0315.v1
zhang, C.; Asif, H.; Calcagno, T. M.; Kumar, N.; Fregien, N. L.; Mirsaeidi, M. Indoor PM10 Upregulates Pro-inflammatory Mediators in Bronchial Epithelial Cells. Preprints2020, 2020080315. https://doi.org/10.20944/preprints202008.0315.v1
APA Style
zhang, C., Asif, H., Calcagno, T. M., Kumar, N., Fregien, N. L., & Mirsaeidi, M. (2020). Indoor PM<sub>10</sub> Upregulates Pro-inflammatory Mediators in Bronchial Epithelial Cells. Preprints. https://doi.org/10.20944/preprints202008.0315.v1
Chicago/Turabian Style
zhang, C., Nevis L Fregien and Mehdi Mirsaeidi. 2020 "Indoor PM<sub>10</sub> Upregulates Pro-inflammatory Mediators in Bronchial Epithelial Cells" Preprints. https://doi.org/10.20944/preprints202008.0315.v1
Abstract
Indoor dusts are collectively formed from anthropogenic and atmospheric activities. Particle matter 10 (PM10) is inhalable and causes significant inflammation by interaction with the pulmonary epithelial barrier. The mediators involved in bronchial epithelial cells response to dust are remined unknown. The air-liquid interface of our lung on chip model was exposed to indoor dust collected from highly polluted houses in Delhi, India. The media were collected after 4 days and cytokine levels were measured. We found that the concentration of IFN, IFNγ, Interleukin-6 (IL-6), IL1b, TNFa, and Granulocyte monocyte colony stimulating factor (GM-CSF) were significantly increased after exposure to indoor dust. IFN type I pathways were a major response from dust exposure. Further investigation is needed to determine the mechanism of action and targets of dust in bronchial epithelial cells.
Keywords
Indoor; PM10; pulmonary disease; inflammation; IFN; type I interferon; cytokine; epithelial cell
Subject
Medicine and Pharmacology, Pharmacology and Toxicology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.