Inflammatory response to chronic nicotine-containing electronic cigarette exposure in a rat model of myocardial infarction
Introduction The long-term effects of chronic electronic cigarette (e-cigarette) exposure on lung and heart inflammation during the healing phase of myocardial infarction (MI) remain unexplored. Additionally, the impact of e-cigarette exposure on blood parameters in this context is unclear. This stu...
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| Main Authors: | , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
European Publishing
2025-05-01
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| Series: | Tobacco Induced Diseases |
| Subjects: | |
| Online Access: | https://www.tobaccoinduceddiseases.org/Inflammatory-response-to-chronic-nicotine-containing-electronic-cigarette-exposure,204010,0,2.html |
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| Summary: | Introduction
The long-term effects of chronic electronic cigarette (e-cigarette)
exposure on lung and heart inflammation during the healing phase of myocardial
infarction (MI) remain unexplored. Additionally, the impact of e-cigarette
exposure on blood parameters in this context is unclear. This study aims to assess
e-cigarette with nicotine (e-cig Nic+) effects on lung histology, inflammatory gene
expression in cardiac tissue, and blood parameters during MI recovery
Methods
Sprague Dawley rats of both sexes underwent proximal left coronary artery
occlusion to induce a large anterior wall MI. After one week, rats were randomized
to either air or e-cig Nic+ exposure for 12 weeks.
Results
In the lungs, e-cig Nic+ exposure led to a significant accumulation of
inflammatory cells within the alveolar spaces and increased inflammatory cell
numbers in the lung parenchyma compared to the air group. Numerically elevated levels of
malondialdehyde (MDA), an oxidative stress biomarker, were observed in the
e-cig Nic+ group. In the heart, a PCR array analysis of inflammatory cytokines
and receptors revealed that 70 out of 84 inflammatory-related genes were
downregulated in the e-cig Nic+ group, with 11 reaching statistical significance.
Additionally, the blood of rats exposed to e-cig Nic+ exhibited significantly lower white blood
cell, lymphocyte, and platelet counts compared to the air group.
Conclusions
Chronic exposure to e-cig Nic+ exacerbates lung inflammation, alters
inflammatory gene expression in the heart, and suppresses immune cell counts
in the blood during MI recovery. These findings suggest that e-cigarette with
nicotine aerosol inhalation contributes to lung lesions and dampens immune and
inflammatory responses in an already compromised MI setting. |
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| ISSN: | 1617-9625 |