Gasoline fume inhalation induces apoptosis, inflammation, and favors Th2 polarization in C57BL/6 mice

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dc.contributor.author Nour-Eldine, Wared
dc.contributor.author Sayyed, Katia
dc.contributor.author Harhous, Zeina
dc.contributor.author Dagher-Hamalian, Carole
dc.contributor.author Mehanna, Stephanie
dc.contributor.author Achkouti, Donna
dc.contributor.author ElKazzaz, Hanan
dc.contributor.author Khnayzer, Rony S.
dc.contributor.author Kobeissy, Firas
dc.contributor.author Khalil, Christian
dc.contributor.author Abi-Gerges, Aniella
dc.date.accessioned 2023-01-09T13:44:35Z
dc.date.available 2023-01-09T13:44:35Z
dc.date.copyright 2022 en_US
dc.date.issued 2023-01-09
dc.identifier.issn 0260-437X en_US
dc.identifier.uri http://hdl.handle.net/10725/14354
dc.description.abstract Gasoline exposure has been widely reported in the literature as being toxic to human health. However, the exact underlying molecular mechanisms triggered by its inhalation have not been thoroughly investigated. We herein present a model of sub-chronic, static gasoline vapor inhalation in adult female C57BL/6 mice. Animals were exposed daily to either gasoline vapors (0.86 g/animal/90 min) or ambient air for 5 days/week over 7 consecutive weeks. At the end of the study period, toxic and molecular mechanisms underlying the inflammatory, oxidative, and apoptotic effects triggered by gasoline vapors, were examined in the lungs and liver of gasoline-exposed (GE) mice. Static gasoline exposure induced a significant increase (+21%) in lungs/body weight (BW) ratio in GE versus control (CON) mice along with a pulmonary inflammation attested by histological staining. The latter was consistent with increases in the transcript levels of proinflammatory cytokines [Interleukins (ILs) 4 and 6], respectively by ~ 6- and 4-fold in the lungs of GE mice compared to CON. Interestingly, IL-10 expression was also increased by ~ 10-fold in the lungs of GE mice suggesting an attempt to counterbalance the established inflammation. Moreover, the pulmonary expression of IL-12 and TNF-α was downregulated by 2- and 4-fold, respectively, suggesting the skewing toward Th2 phenotype. Additionally, GE mice showed a significant upregulation in Bax/Bcl-2 ratio, caspases 3, 8, and 9 with no change in JNK expression in the lungs, suggesting the activation of both intrinsic and extrinsic apoptotic pathways. Static gasoline exposure over seven consecutive weeks had a minor hepatic portal inflammation attested by H&E staining along with an increase in the hepatic expression of the mitochondrial complexes in GE mice. Therefore, tissue damage biomarkers highlight the health risks associated with vapor exposure and may present potential therapeutic targets for recovery from gasoline intoxication. en_US
dc.language.iso en en_US
dc.title Gasoline fume inhalation induces apoptosis, inflammation, and favors Th2 polarization in C57BL/6 mice en_US
dc.type Article en_US
dc.description.version Published en_US
dc.author.school SOM en_US
dc.author.school SAS
dc.author.idnumber 200501196 en_US
dc.author.idnumber 201402416 en_US
dc.author.department N/A en_US
dc.author.department Natural Sciences
dc.relation.journal Journal of Applied Toxicology en_US
dc.journal.volume 42 en_US
dc.journal.issue 7 en_US
dc.article.pages 1178-1191 en_US
dc.keywords Antioxidant enzymes en_US
dc.keywords Apoptosis en_US
dc.keywords Gasoline inhalation en_US
dc.keywords Inflammation en_US
dc.keywords Th2 polarization en_US
dc.identifier.doi https://doi.org/10.1002/jat.4286 en_US
dc.identifier.ctation Nour‐Eldine, W., Sayyed, K., Harhous, Z., Dagher‐Hamalian, C., Mehanna, S., Achkouti, D., ... & Abi‐Gerges, A. (2022). Gasoline fume inhalation induces apoptosis, inflammation, and favors Th2 polarization in C57BL/6 mice. Journal of Applied Toxicology, 42(7), 1178-1191. en_US
dc.author.email rony.khnayzer@lau.edu.lb en_US
dc.author.email aniella.abigerges@lau.edu.lb en_US
dc.identifier.tou http://libraries.lau.edu.lb/research/laur/terms-of-use/articles.php en_US
dc.identifier.url https://analyticalsciencejournals.onlinelibrary.wiley.com/doi/full/10.1002/jat.4286 en_US
dc.orcid.id https://orcid.org/0000-0001-7775-0027 en_US
dc.orcid.id https://orcid.org/0000-0001-9974-4023 en_US
dc.author.affiliation Lebanese American University en_US

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