Effects of combustible cigarettes and electronic nicotine delivery systems on the development and progression of chronic lung inflammation in mice.

Kastratovic, Nikolina; Markovic, Vladimir; Harrell, Carl Randall; Arsenijevic, Aleksandar; Stojanovic, Milica Dimitrijevic; Djonov, Valentin; Volarevic, Vladislav (2024). Effects of combustible cigarettes and electronic nicotine delivery systems on the development and progression of chronic lung inflammation in mice. Nicotine & tobacco research, 26(6), pp. 704-714. Oxford University Press 10.1093/ntr/ntad235

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INTRODUCTION

Although detrimental effects of combustible cigarettes (CCs) on the progression of lung inflammatory diseases are well known, changes in electronic nicotine delivery systems (ENDS)-exposed lung-infiltrated immune cells are still unrevealed.

METHODS

The analysis of blood gas parameters, descriptive and quantitative histology of lung tissues, determination of serum cytokines, intracellular staining and flow cytometry analysis of lung-infiltrated immune cells were used to determine the differences in the extent of lung injury and inflammation between mice from experimental (CC and ENDS-exposed animals) and control group (Air-exposed mice).

RESULTS

Continuous exposition to either CCs or ENDS induced severe systemic inflammatory response, increased activation of NLRP3 inflammasome in neutrophils and macrophages and enhanced dendritic cell-dependent activation of Th1 and Th17 cells in the lungs. ENDS induced less severe immune response than CCs. Serum concentrations of inflammatory cytokines were significantly lower in the samples of ENDS-exposed mice. Compared to CCs, ENDS recruited lower number of circulating leukocytes in injured lungs and had less capacity to induce CD14/TLR-2-dependent activation of NLRP3 inflammasome in lung-infiltrated neutrophils and macrophages. ENDS-primed dendritic cells had reduced capacity for the generation of Th1 and Th17 cell-driven lung inflammation. Accordingly, extensive immune cell-driven lung injury resulted in severe respiratory dysfunction in CCs-exposed mice, while ENDS caused moderate respiratory dysfunction in experimental animals.

CONCLUSIONS

Continuous exposition to either CCs or ENDS induced immune cell-driven lung damage in mice. ENDS triggered immune response which was less potent than inflammatory response elicited by CCs and, therefore, caused less severe lung injury and inflammation.

IMPLICATIONS

This is the first study that compared the effects of CCs and ENDS on lung-infiltrated immune cells. Although both CCs and ENDS elicited systemic inflammatory response, immune cell-driven lung injury and inflammation were less severe in ENDS-exposed than in CC-exposed animals. Continuous exposition to ENDS-sourced aerosols was less harmful for respiratory function of experimental animals than CC-derived smoke.

Item Type:	Journal Article (Original Article)
Division/Institute:	04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Anatomy 04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Anatomy > Topographical and Clinical Anatomy
UniBE Contributor:	Djonov, Valentin Georgiev
Subjects:	500 Science > 570 Life sciences; biology 600 Technology > 610 Medicine & health
ISSN:	1469-994X
Publisher:	Oxford University Press
Language:	English
Submitter:	Pubmed Import
Date Deposited:	30 Nov 2023 10:52
Last Modified:	23 May 2024 00:12
Publisher DOI:	10.1093/ntr/ntad235
PubMed ID:	38018885
Uncontrolled Keywords:	combustible cigarettes electronic nicotine delivery systems immune cells lung injury and inflammation
URI:	https://boris.unibe.ch/id/eprint/189641