The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
E-Cigarette Use Causes a Unique Innate Immune Response in the Lung, Involving Increased Neutrophilic Activation and Altered Mucin Secretion
Open accessAbstract
RATIONALE: E-cigarettes have become increasingly popular and little is known about their potential adverse health effects. OBJECTIVES: To determine the effects of e-cigarette use on the airways. METHODS: Induced sputum samples from cigarette smokers, e-cigarette users, and nonsmokers were analyzed by quantitative proteomics, and the total and individual concentrations of mucins MUC5AC and MUC5B were determined by light scattering/refractometry and labeled mass spectrometry, respectively. Neutrophil extracellular trap (NET) formation rates were also determined for the same groups. MEASUREMENTS AND MAIN RESULTS: E-cigarette users exhibited significant increases in aldehyde-detoxification and oxidative stress-related proteins associated with cigarette smoke compared with nonsmokers. The levels of innate defense proteins associated with chronic obstructive pulmonary disease, such as elastase and matrix metalloproteinase-9, were significantly elevated in e-cigarette users as well. E-cigarette users' sputum also uniquely exhibited significant increases in neutrophil granulocyte-related and NET-related proteins, such as myeloperoxidase, azurocidin, and protein-arginine deiminase 4, despite no significant elevation in neutrophil cell counts. Peripheral neutrophils from e-cigarette users showed increased susceptibility to phorbol 12-myristate 13-acetate-induced NETosis. Finally, a compositional change in the gel-forming building blocks of airway mucus (i.e., an elevated concentration of mucin MUC5AC) was observed in both cigarette smokers and e-cigarette users. CONCLUSIONS: Together, our results indicate that e-cigarette use alters the profile of innate defense proteins in airway secretions, inducing similar and unique changes relative to cigarette smoking. These data challenge the concept that e-cigarettes are a healthier alternative to cigarettes.
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Cited by
What are the respiratory effects of e-cigarettes?
Gotts, J. E., Jordt, S.-E., McConnell, R., & Tarran, R. (2019) · BMJ · doi:10.1136/bmj.l5275 · Cited by 516
Electronic cigarettes disrupt lung lipid homeostasis and innate immunity independent of nicotine
Madison, M. C., Landers, C. T., Gu, B.-H., Chang, C.-Y., Tung, H.-Y., You, R., Hong, M. J., Baghaei, N., Song, L.-Z., Porter, P., et al. (2019) · Journal of Clinical Investigation · doi:10.1172/jci128531 · Cited by 391
Role of inflammatory cells in airway remodeling in COPD
Wang, Y., Xu, J., Meng, Y., Adcock, I. M., & Yao, X. (2018) · International Journal of Chronic Obstructive Pulmonary Disease · doi:10.2147/copd.s176122 · Cited by 373
Association of E-Cigarette Use With Respiratory Disease Among Adults: A Longitudinal Analysis
Bhatta, D. N., & Glantz, S. A. (2020) · American Journal of Preventive Medicine · doi:10.1016/j.amepre.2019.07.028 · Cited by 292
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Metadata
- Authors
- Reidel, B., Radicioni, G., Clapp, P. W., Ford, A. A., Abdelwahab, S., Rebuli, M. E., Haridass, P., Alexis, N. E., Jaspers, I., & Kesimer, M.
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 2018-02-15
- Volume
- 197
- Issue
- 4
- Pages
- 492-501
- ISSN
- 1073-449X (ISSN-L)
- 1535-4970
- OpenAlex
- W2766814588
- Cited by
- 375
- References
- 45
- FWCI
- 23.86
- Type
- journal article
- Language
- en
- Open access
- green
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- Reidel, B., Radicioni, G., Clapp, P. W., Ford, A. A., Abdelwahab, S., Rebuli, M. E., Haridass, P., Alexis, N. E., Jaspers, I., & Kesimer, M. (2018). E-Cigarette Use Causes a Unique Innate Immune Response in the Lung, Involving Increased Neutrophilic Activation and Altered Mucin Secretion. American Journal of Respiratory and Critical Care Medicine. https://doi.org/10.1164/rccm.201708-1590oc
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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