Chronic Exposure to Flavored Tobacco Aerosols Induces Inflammation and Hepatic Mitochondrial Impairment in Pregnant Versus Non-Pregnant Mouse Cohorts
8 affiliations
- 1Department of Pediatrics, Division of Pediatric Cardiology, Saint Louis University, St. Louis, MO 63104, USA
- 2Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA
- 3Department of Biochemistry, Saint Louis University, St. Louis, MO 63104, USA
- 4Department of Occupational and Environmental Health, University of Iowa, Iowa City, IA 52242, USA
- 5Department of Pediatrics, Division of Pediatric Cardiology, Carver College of Medicine, Iowa City, IA 52242, USA
- 6Department of Studies and Research in Biochemistry, Tumkur University, Tumkur 572118, Karnataka, India
- 7Department of Medicine, Vanderbilt University Medical Center, Nashville 37232, TN, USA
- 8American Heart Association, Dallas, TX 75231, USA
Abstract
This study was conducted to investigate the impact of Virginia tobacco (VT), Menthol (MT), and sham aerosols on both normal and pathological responses in pregnant and non-pregnant mouse groups. Aerosol vaping exposure and body weight analysis were evaluated in pregnant and non-pregnant cohorts and compared with controls exposed to sham aerosols in each group. We assessed pulmonary inflammation using the Bronchoalveolar Lavage Fluid (BALF) total cell count, total protein, and lactate dehydrogenase (LDH) activity. In addition, we measured hepatic triglyceride levels and lipogenic genes in the liver, such as Scd1, Fasn, Srebp1c1, and the estrogen receptor (Esr1), via RT-qPCR and Western blot analysis. Liver fibrosis was assessed via histopathology and mitochondrial functional assays, and serum cytokines were measured in each group. In pregnant mice exposed to VT, pulmonary inflammation, increased cell counts and protein content, and no change in lactate dehydrogenase activity in Bronchoalveolar Lavage Fluid (BALF) were observed compared with non-pregnant mice. VT exposure appeared to cause direct adverse health outcomes leading to increased expression of liver lipogenic genes, such as Scd1, Fasn, Srebp1c, and estrogen receptors. Maternal liver lipid equilibrium was disrupted upon VT exposure. Vaping either VT or MT significantly reduced mitochondrial oxidative function in the livers of pregnant mice but not in those of non-pregnant mice. This study’s findings suggest that pregnancy may be associated with distinct immunological responses to VT and MT exposure. VT exposure was associated with altered hepatic lipogenic gene expression, suggesting potential metabolic effects on the maternal liver, whereas MT exposure was associated with liver structural changes and fibrosis-related outcomes.
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BibTeX
@article{sample2026chronic,
title = {{Chronic Exposure to Flavored Tobacco Aerosols Induces Inflammation and Hepatic Mitochondrial Impairment in Pregnant Versus Non-Pregnant Mouse Cohorts}},
author = {Kamryn Sample and Manjula M. Venkatappa and Young Do Koo and Zachary Foulks and Vingie Ng and Morgan Shaffer and Mei L. Lietsch and Andrea Adamcakova-Dodd and Peter S. Thorne and Kyle S. McCommis and Devaraja Sannaningaiah and Rose M. Robertson and Vernat Exil},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = nov,
doi = {10.3390/ijms27219851},
url = {https://www.mdpi.com/1422-0067/27/21/9851},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Chronic Exposure to Flavored Tobacco Aerosols Induces Inflammation and Hepatic Mitochondrial Impairment in Pregnant Versus Non-Pregnant Mouse Cohorts
AU - Kamryn Sample
AU - Manjula M. Venkatappa
AU - Young Do Koo
AU - Zachary Foulks
AU - Vingie Ng
AU - Morgan Shaffer
AU - Mei L. Lietsch
AU - Andrea Adamcakova-Dodd
AU - Peter S. Thorne
AU - Kyle S. McCommis
AU - Devaraja Sannaningaiah
AU - Rose M. Robertson
AU - Vernat Exil
PY - 2026
DA - 2026/11/03
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219851
UR - https://www.mdpi.com/1422-0067/27/21/9851
AB - This study was conducted to investigate the impact of Virginia tobacco (VT), Menthol (MT), and sham aerosols on both normal and pathological responses in pregnant and non-pregnant mouse groups. Aerosol vaping exposure and body weight analysis were evaluated in pregnant and non-pregnant cohorts and compared with controls exposed to sham aerosols in each group. We assessed pulmonary inflammation using the Bronchoalveolar Lavage Fluid (BALF) total cell count, total protein, and lactate dehydrogenase (LDH) activity. In addition, we measured hepatic triglyceride levels and lipogenic genes in the liver, such as Scd1, Fasn, Srebp1c1, and the estrogen receptor (Esr1), via RT-qPCR and Western blot analysis. Liver fibrosis was assessed via histopathology and mitochondrial functional assays, and serum cytokines were measured in each group. In pregnant mice exposed to VT, pulmonary inflammation, increased cell counts and protein content, and no change in lactate dehydrogenase activity in Bronchoalveolar Lavage Fluid (BALF) were observed compared with non-pregnant mice. VT exposure appeared to cause direct adverse health outcomes leading to increased expression of liver lipogenic genes, such as Scd1, Fasn, Srebp1c, and estrogen receptors. Maternal liver lipid equilibrium was disrupted upon VT exposure. Vaping either VT or MT significantly reduced mitochondrial oxidative function in the livers of pregnant mice but not in those of non-pregnant mice. This study’s findings suggest that pregnancy may be associated with distinct immunological responses to VT and MT exposure. VT exposure was associated with altered hepatic lipogenic gene expression, suggesting potential metabolic effects on the maternal liver, whereas MT exposure was associated with liver structural changes and fibrosis-related outcomes.
SN - 1422-0067
ER -