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Related Experiment Video

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Production of Genetically Engineered Golden Syrian Hamsters by Pronuclear Injection of the CRISPR/Cas9 Complex
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Acute vaping in a golden Syrian hamster causes inflammatory response transcriptomic changes.

Daniel M Hinds1, Heidi J Nick2,3, Tessa M Vallin2

  • 1Department of Pediatrics, University of Iowa, Iowa City, Iowa.

American Journal of Physiology. Lung Cellular and Molecular Physiology
|August 30, 2022
PubMed
Summary

E-cigarette vaping, even acutely, causes significant gene expression changes in the respiratory tract of Syrian hamsters. This study demonstrates the hamster as a viable model for vaping research, revealing impacts on inflammation, fibrosis, and coagulation pathways.

Keywords:
E-cigarettegolden Syrian hamsterproinflammatorytissue factorvaping

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Area of Science:

  • Respiratory Medicine
  • Toxicology
  • Animal Models

Background:

  • E-cigarette vaping is a prevalent form of nicotine consumption, particularly among youth.
  • While marketed as safer than smoking, vaping induces proinflammatory changes in respiratory tracts of rodent models.
  • A suitable acute vaping exposure model in hamsters, known for respiratory virus susceptibility, was lacking.

Purpose of the Study:

  • To establish and validate the golden Syrian hamster as a model for acute e-cigarette vaping exposure.
  • To investigate the molecular and cellular changes in the respiratory tract following a 2-day vaping protocol.
  • To assess the impact of nicotine-dependent and independent pathways on gene expression.

Main Methods:

  • Male golden Syrian hamsters underwent a 2-day whole-body vaping exposure.
  • Evaluated serum cotinine levels, bronchoalveolar lavage cells, and nasal/lung histopathology.
  • Utilized reverse transcription-quantitative polymerase chain reaction (RT-qPCR) for gene expression analysis in nasopharynx and lung.

Main Results:

  • Nasal tissue showed nicotine-dependent increases in inflammation (CCL-5, CXCL-10) and fibrosis (TGF-β) genes.
  • Lung tissue exhibited nicotine-dependent upregulation of genes in renin-angiotensin (ACE, ACE2), coagulation (tissue factor), and inflammation pathways.
  • Vaping induced nicotine-independent changes in oxidative stress (SOD-2) and angiogenesis (VEGF-A) in both nasal and lung tissues.

Conclusions:

  • The Syrian hamster is confirmed as a viable model for studying acute e-cigarette vaping effects.
  • Acute vaping exposure significantly upregulates mRNAs in the respiratory tract, impacting multiple critical biological pathways.
  • This study is the first to report increased lung tissue factor gene expression following e-cigarette vaping.