The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
Electronic cigarettes disrupt lung lipid homeostasis and innate immunity independent of nicotine
Open accessAbstract
Electronic nicotine delivery systems (ENDS) or e-cigarettes have emerged as a popular recreational tool among adolescents and adults. Although the use of ENDS is often promoted as a safer alternative to conventional cigarettes, few comprehensive studies have assessed the long-term effects of vaporized nicotine and its associated solvents, propylene glycol (PG) and vegetable glycerin (VG). Here, we show that compared with smoke exposure, mice receiving ENDS vapor for 4 months failed to develop pulmonary inflammation or emphysema. However, ENDS exposure, independent of nicotine, altered lung lipid homeostasis in alveolar macrophages and epithelial cells. Comprehensive lipidomic and structural analyses of the lungs revealed aberrant phospholipids in alveolar macrophages and increased surfactant-associated phospholipids in the airway. In addition to ENDS-induced lipid deposition, chronic ENDS vapor exposure downregulated innate immunity against viral pathogens in resident macrophages. Moreover, independent of nicotine, ENDS-exposed mice infected with influenza demonstrated enhanced lung inflammation and tissue damage. Together, our findings reveal that chronic e-cigarette vapor aberrantly alters the physiology of lung epithelial cells and resident immune cells and promotes poor response to infectious challenge. Notably, alterations in lipid homeostasis and immune impairment are independent of nicotine, thereby warranting more extensive investigations of the vehicle solvents used in e-cigarettes.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
IRF-7 is the master regulator of type-I interferon-dependent immune responses
Honda, K., Yanai, H., Negishi, H., Asagiri, M., Sato, M., Mizutani, T., Shimada, N., Ohba, Y., Takaoka, A., Yoshida, N., et al. (2005) · Nature · doi:10.1038/nature03464 · Cited by 2,245
the Immunological Genome Consortium, Gautier, E. L., Shay, T., Miller, J., Greter, M., Jakubzick, C., Ivanov, S., Helft, J., Chow, A., Elpek, K. G., et al. (2012) · Nature Immunology · doi:10.1038/ni.2419 · Cited by 1,972 · cited 1×
“Gene expression profiling of resident alveolar macrophages is consistent with an enrichment of genes associated with lipid metabolism, thus highlighting their significant role in pulmonary surfactant homeostasis (36, 37).”
BackgroundAlveolar macrophages: plasticity in a tissue-specific context
Hussell, T., & Bell, T. J. (2014) · Nature Reviews Immunology · doi:10.1038/nri3600 · Cited by 1,377
Soneji, S., Barrington-Trimis, J. L., Wills, T. A., Leventhal, A. M., Unger, J. B., Gibson, L. A., Yang, J., Primack, B. A., Andrews, J. A., Miech, R. A., et al. (2017) · JAMA Pediatrics · doi:10.1001/jamapediatrics.2017.1488 · Cited by 1,170
Immunoregulatory functions of surfactant proteins
Wright, J. R. (2005) · Nature Reviews Immunology · doi:10.1038/nri1528 · Cited by 964
Four hundred and sixty brands of e-cigarettes and counting: implications for product regulation
Zhu, S.-H., Sun, J. Y., Bonnevie, E., Cummins, S. E., Gamst, A., Yin, L., & Lee, M. (2014) · Tobacco Control · doi:10.1136/tobaccocontrol-2014-051670 · Cited by 913
Pulmonary Alveolar Proteinosis
Trapnell, B. C., Whitsett, J. A., & Nakata, K. (2003) · New England Journal of Medicine · doi:10.1056/nejmra023226 · Cited by 790
Vital Signs: Tobacco Product Use Among Middle and High School Students — United States, 2011–2018
Gentzke, A. S., Creamer, M., Cullen, K. A., Ambrose, B. K., Willis, G., Jamal, A., & King, B. A. (2019) · MMWR. Morbidity and Mortality Weekly Report · doi:10.15585/mmwr.mm6806e1 · Cited by 766
Lerner, C. A., Sundar, I. K., Yao, H., Gerloff, J., Ossip, D. J., McIntosh, S., Robinson, R., & Rahman, I. (2015) · PLOS ONE · doi:10.1371/journal.pone.0116732 · Cited by 666
GM-CSF Regulates Alveolar Macrophage Differentiation and Innate Immunity in the Lung through PU.1
Shibata, Y., Berclaz, P.-Y., Chroneos, Z. C., Yoshida, M., Whitsett, J. A., & Trapnell, B. C. (2001) · Immunity · doi:10.1016/s1074-7613(01)00218-7 · Cited by 618
Cited by
Collision of the COVID-19 and Addiction Epidemics
Volkow, N. D. (2020) · Annals of Internal Medicine · doi:10.7326/m20-1212 · Cited by 734
Potential for Release of Pulmonary Toxic Ketene from Vaping Pyrolysis of Vitamin E Acetate
Wu, D., & O’Shea, D. F. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1920925117 · Cited by 137
E-cigarette vaping associated acute lung injury (EVALI): state of science and future research needs
Marrocco, A., Singh, D., Christiani, D. C., & Demokritou, P. (2022) · Critical Reviews in Toxicology · doi:10.1080/10408444.2022.2082918 · Cited by 78
“Yet, since lipid-laden macrophages were characterized in mice exposed to e-cig vapors generated from PG and VG regardless of the presence of nicotine or VEA as a result of the alteration of lipid homeostasis (Madison et al. 2019), as well as in lungs of individuals exposed to other chemicals and healthy smokers (Maddo…”
Background
Metadata
- Authors
- 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., Putluri, N., Salas, R., Gilbert, B. E., Levental, I., Campen, M. J., Corry, D. B., & Kheradmand, F.
- Venue
- Journal of Clinical Investigation
- Published
- 2019-09-04
- Volume
- 129
- Issue
- 10
- Pages
- 4290-4304
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- OpenAlex
- W2972010736
- Cited by
- 391
- References
- 57
- FWCI
- 35.15
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Electronic cigarettes disrupt lung lipid homeostasis and innate immunity independent of nicotine. https://app.cochat.ai/papers/10.1172/jci128531
- The paper
- 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., Putluri, N., Salas, R., Gilbert, B. E., Levental, I., Campen, M. J., Corry, D. B., & Kheradmand, F. (2019). Electronic cigarettes disrupt lung lipid homeostasis and innate immunity independent of nicotine. Journal of Clinical Investigation. https://doi.org/10.1172/jci128531
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
