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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| Format: | Article |
| Language: | English |
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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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| _version_ | 1849708870609403904 |
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| author | Jianru Shi Wangde Dai Juan Carreno Jaspreet Sachdeva Jesus Chavez Michael T. Kleinman David A. Herman Rebecca J. Arechavala Irene Hasen Amanda Ting Robert A. Kloner |
| author_facet | Jianru Shi Wangde Dai Juan Carreno Jaspreet Sachdeva Jesus Chavez Michael T. Kleinman David A. Herman Rebecca J. Arechavala Irene Hasen Amanda Ting Robert A. Kloner |
| author_sort | Jianru Shi |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-c3b5dd97acb24f4c8d74717bff2e45b1 |
| institution | DOAJ |
| issn | 1617-9625 |
| language | English |
| publishDate | 2025-05-01 |
| publisher | European Publishing |
| record_format | Article |
| series | Tobacco Induced Diseases |
| spelling | doaj-art-c3b5dd97acb24f4c8d74717bff2e45b12025-08-20T03:15:31ZengEuropean PublishingTobacco Induced Diseases1617-96252025-05-0123May11110.18332/tid/204010204010Inflammatory response to chronic nicotine-containing electronic cigarette exposure in a rat model of myocardial infarctionJianru Shi0Wangde Dai1Juan Carreno2Jaspreet Sachdeva3Jesus Chavez4Michael T. Kleinman5David A. Herman6Rebecca J. Arechavala7Irene Hasen8Amanda Ting9Robert A. Kloner10Cardiovascular Research Institute, Huntington Medical Research Institutes, Pasadena, United StatesCardiovascular Research Institute, Huntington Medical Research Institutes, Pasadena, United StatesCardiovascular Research Institute, Huntington Medical Research Institutes, Pasadena, United StatesCardiovascular Research Institute, Huntington Medical Research Institutes, Pasadena, United StatesCardiovascular Research Institute, Huntington Medical Research Institutes, Pasadena, United StatesDepartment of Environmental and Occupational Health, University of California Irvine, Irvine, United StatesDepartment of Environmental and Occupational Health, University of California Irvine, Irvine, United StatesDepartment of Environmental and Occupational Health, University of California Irvine, Irvine, United StatesDepartment of Environmental and Occupational Health, University of California Irvine, Irvine, United StatesDepartment of Environmental and Occupational Health, University of California Irvine, Irvine, United StatesCardiovascular Research Institute, Huntington Medical Research Institutes, Pasadena, United StatesIntroduction 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.https://www.tobaccoinduceddiseases.org/Inflammatory-response-to-chronic-nicotine-containing-electronic-cigarette-exposure,204010,0,2.htmle-cigarettelung inflammationcardiac inflammatory genesblood parameters |
| spellingShingle | Jianru Shi Wangde Dai Juan Carreno Jaspreet Sachdeva Jesus Chavez Michael T. Kleinman David A. Herman Rebecca J. Arechavala Irene Hasen Amanda Ting Robert A. Kloner Inflammatory response to chronic nicotine-containing electronic cigarette exposure in a rat model of myocardial infarction Tobacco Induced Diseases e-cigarette lung inflammation cardiac inflammatory genes blood parameters |
| title | Inflammatory response to chronic nicotine-containing electronic cigarette exposure in a rat model of myocardial infarction |
| title_full | Inflammatory response to chronic nicotine-containing electronic cigarette exposure in a rat model of myocardial infarction |
| title_fullStr | Inflammatory response to chronic nicotine-containing electronic cigarette exposure in a rat model of myocardial infarction |
| title_full_unstemmed | Inflammatory response to chronic nicotine-containing electronic cigarette exposure in a rat model of myocardial infarction |
| title_short | Inflammatory response to chronic nicotine-containing electronic cigarette exposure in a rat model of myocardial infarction |
| title_sort | inflammatory response to chronic nicotine containing electronic cigarette exposure in a rat model of myocardial infarction |
| topic | e-cigarette lung inflammation cardiac inflammatory genes blood parameters |
| url | https://www.tobaccoinduceddiseases.org/Inflammatory-response-to-chronic-nicotine-containing-electronic-cigarette-exposure,204010,0,2.html |
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