Acute Effects of Heated Tobacco Product (IQOS) Aerosol Inhalation on Lung Tissue Damage and Inflammatory Changes in the Lungs.

Autor:	Bhat TA; Department of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY., Kalathil SG; Department of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY., Leigh N; Department of Health Behavior, Roswell Park Comprehensive Cancer Center, Buffalo, NY., Muthumalage T; Department of Environmental Medicine, University of Rochester Medical Center, School of Medicine and Dentistry, Rochester, NY., Rahman I; Department of Environmental Medicine, University of Rochester Medical Center, School of Medicine and Dentistry, Rochester, NY., Goniewicz ML; Department of Health Behavior, Roswell Park Comprehensive Cancer Center, Buffalo, NY., Thanavala YM; Department of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY.
Jazyk:	angličtina
Zdroj:	Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco [Nicotine Tob Res] 2021 Jun 08; Vol. 23 (7), pp. 1160-1167.
DOI:	10.1093/ntr/ntaa267
Abstrakt:	Introduction: Emerging heated tobacco products (HTPs) were designed to reduce exposure to toxicants from cigarette smoke (CS) by avoiding burning tobacco and instead heating tobacco. We studied the effects of short-term inhalation of aerosols emitted from HTP called IQOS, on lung damage and immune-cell recruitment to the lungs in mice. Methods: Numerous markers of lung damage and inflammation including albumin and lung immune-cell infiltrates, proinflammatory cytokines, and chemokines were quantified in lungs and bronchoalveolar (BAL) fluid from IQOS, CS, or air-exposed (negative control) mice. Results: Importantly, as a surrogate marker of lung epithelial-cell damage, we detected significantly increased levels of albumin in the BAL fluid of both HTP- and CS-exposed mice compared with negative controls. Total numbers of leukocytes infiltrating the lungs were equivalent following both IQOS aerosols and CS inhalation and significantly increased compared with air-exposed controls. We also observed significantly increased numbers of CD4+IL-17A+ T cells, a marker of a T-cell immune response, in both groups compared with air controls; however, numbers were the highest following CS exposure. Finally, the numbers of CD4+RORγt+ T cells, an inflammatory T-cell subtype expressing the transcription factor that is essential for promoting differentiation into proinflammatory Th17 cells, were significantly augmented in both groups compared with air-exposed controls. Levels of several cytokines in BAL were significantly elevated, reflecting a proinflammatory milieu. Conclusions: Our study demonstrates that short-term inhalation of aerosols from IQOS generates damage and proinflammatory changes in the lung that are substantially similar to that elicited by CS exposure. Implications: Exposure of mice to IQOS, one of the candidate modified-risk tobacco products, induces inflammatory immune-cell accumulation in the lungs and augments the levels of proinflammatory cytokines and chemokines in the BAL fluid. Such an exacerbated pulmonary proinflammatory microenvironment is associated with lung epithelial-cell damage in IQOS-exposed mice, suggesting a potential association with the impairment of lung function. (© The Author(s) 2020. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)
Databáze:	MEDLINE
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