Role of diabetes in lung injury from acute exposure to electronic cigarette, heated tobacco product, and combustible cigarette aerosols in an animal model.
Aerosols
/ adverse effects
Albumins
/ analysis
Animals
Bronchoalveolar Lavage Fluid
/ chemistry
Cigarette Smoking
/ adverse effects
Diabetes Mellitus, Type 2
/ pathology
Disease Models, Animal
Electronic Nicotine Delivery Systems
Female
Interleukin-6
/ genetics
Lung
/ metabolism
Lung Injury
/ etiology
Mice
Mice, Transgenic
Oxidative Stress
Reactive Oxygen Species
/ metabolism
Tobacco Products
/ adverse effects
Tumor Necrosis Factor-alpha
/ genetics
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2021
2021
Historique:
received:
17
11
2020
accepted:
26
07
2021
entrez:
10
8
2021
pubmed:
11
8
2021
medline:
15
12
2021
Statut:
epublish
Résumé
Patients with diabetes are more vulnerable to the detrimental respiratory effects of combustible cigarette smoke (CS) when compared to the general population. Electronic cigarettes (ECIG) and heated tobacco products (HTP) are marketed as less harmful alternatives to CS. In this study, we compared the effects of acute ECIG, HTP and CS exposure on the lungs of type II diabetes versus non-diabetic mice in an animal model. Type II Diabetic (Diab) and Non-Diabetic (Non-Diab) mice were divided into Control, ECIG, HTP and CS groups. Animals were exposed for 6 hrs./day to either air, ECIG, HTP or CS for seven days. Lung injury was determined by a) histopathology, b) wet to dry ratio, c) albumin concentration in bronchoalveolar lavage fluid, d) expression of TNF-α, IL-6, and IL-1 β, e) reactive oxygen species production (ROS), and f) assessment of cellular apoptosis. Lung histology revealed increased edema and inflammatory cells in diabetic mice exposed to ECIG, HTP and CS. The expression of Inflammatory mediators was, in general, more significant in the Diabetic groups as well. TNF-α expression, for example, was upregulated in Diab + ECIG but not in Non-Diab + ECIG. ROS was significantly increased in Diab + CS, less in Non-Diab + CS and weakly noted in ECIG + Diab. Significant albumin leak was observed in Diab and Non-Diab HTP-exposed animals. CS exposure worsened lung injury in Diab when compared to Non-Diab mice. Comorbid medical conditions like diabetes may amplify ill effects of CS, ECIG or HTP exposure.
Sections du résumé
BACKGROUND
Patients with diabetes are more vulnerable to the detrimental respiratory effects of combustible cigarette smoke (CS) when compared to the general population. Electronic cigarettes (ECIG) and heated tobacco products (HTP) are marketed as less harmful alternatives to CS. In this study, we compared the effects of acute ECIG, HTP and CS exposure on the lungs of type II diabetes versus non-diabetic mice in an animal model.
METHODS
Type II Diabetic (Diab) and Non-Diabetic (Non-Diab) mice were divided into Control, ECIG, HTP and CS groups. Animals were exposed for 6 hrs./day to either air, ECIG, HTP or CS for seven days. Lung injury was determined by a) histopathology, b) wet to dry ratio, c) albumin concentration in bronchoalveolar lavage fluid, d) expression of TNF-α, IL-6, and IL-1 β, e) reactive oxygen species production (ROS), and f) assessment of cellular apoptosis.
RESULTS
Lung histology revealed increased edema and inflammatory cells in diabetic mice exposed to ECIG, HTP and CS. The expression of Inflammatory mediators was, in general, more significant in the Diabetic groups as well. TNF-α expression, for example, was upregulated in Diab + ECIG but not in Non-Diab + ECIG. ROS was significantly increased in Diab + CS, less in Non-Diab + CS and weakly noted in ECIG + Diab. Significant albumin leak was observed in Diab and Non-Diab HTP-exposed animals. CS exposure worsened lung injury in Diab when compared to Non-Diab mice.
CONCLUSION
Comorbid medical conditions like diabetes may amplify ill effects of CS, ECIG or HTP exposure.
Identifiants
pubmed: 34375359
doi: 10.1371/journal.pone.0255876
pii: PONE-D-20-34376
pmc: PMC8354464
doi:
Substances chimiques
Aerosols
0
Albumins
0
Interleukin-6
0
Reactive Oxygen Species
0
Tumor Necrosis Factor-alpha
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0255876Subventions
Organisme : NIDA NIH HHS
ID : P50 DA036105
Pays : United States
Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
Références
Cell Mol Biol (Noisy-le-grand). 2012 Feb 16;58 Suppl:OL1623-31
pubmed: 22340705
Nicotine Tob Res. 2021 Jun 8;23(7):1160-1167
pubmed: 33346355
Diabetes Care. 2009 Nov;32 Suppl 2:S429-31
pubmed: 19875595
Chest. 2010 Aug;138(2):393-406
pubmed: 20348195
Oxid Med Cell Longev. 2017;2017:6063201
pubmed: 29333211
Tob Control. 2018 Nov;27(Suppl 1):s1-s6
pubmed: 30352841
Arch Biochem Biophys. 2015 Oct 1;583:55-64
pubmed: 26254814
World J Biol Chem. 2017 May 26;8(2):120-128
pubmed: 28588755
Eur Respir J. 2008 Oct;32(4):962-9
pubmed: 18579551
Lancet. 2017 May 13;389(10082):1931-1940
pubmed: 28513453
Addiction. 2016 Jun;111(6):1077-83
pubmed: 26802864
Nicotine Tob Res. 2016 May;18(5):613-9
pubmed: 26272212
Lancet. 2017 Sep 16;390(10100):1345-1422
pubmed: 28919119
Tob Control. 2013 Jan;22(1):19-23
pubmed: 22034071
Tob Control. 2016 Apr;25(e1):e10-5
pubmed: 25877377
Food Chem Toxicol. 2015 Jun;80:328-345
pubmed: 25843363
Semin Respir Crit Care Med. 2015 Aug;36(4):575-91
pubmed: 26238643
Nicotine Tob Res. 2015 Feb;17(2):150-7
pubmed: 25187061
Diabetes. 2013 Aug;62(8):2935-47
pubmed: 23557706
J Gen Intern Med. 2005 Dec;20(12):1142-5
pubmed: 16423106
Endocrinol Metab Clin North Am. 2014 Mar;43(1):25-40
pubmed: 24582090