Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD)

ABSTRACT

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide, and its global health burden is increasing. COPD is characterized by emphysema, mucus hypersecretion, and persistent lung inflammation, and clinically by chronic airflow obstruction and symptoms of dyspnea, cough, and fatigue in patients. A cluster of pathologies including chronic bronchitis, emphysema, asthma, and cardiovascular disease in the form of hypertension and atherosclerosis variably coexist in COPD patients. Underlying causes for COPD include primarily tobacco use but may also be driven by exposure to air pollutants, biomass burning, and workplace related fumes and chemicals. While no single animal model might mimic all features of human COPD, a wide variety of published models have collectively helped to improve our understanding of disease processes involved in the genesis and persistence of COPD. In this review, the pathogenesis and associated risk factors of COPD are examined in different mammalian models of the disease. Each animal model included in this review is exclusively created by tobacco smoke (TS) exposure. As animal models continue to aid in defining the pathobiological mechanisms of and possible novel therapeutic interventions for COPD, the advantages and disadvantages of each animal model are discussed.

KEYWORDS:

• chronic obstructive pulmonary disease (COPD)
• animal models
• emphysema
• chronic bronchitis
• tobacco smoke

Acknowledgments

We thank the editorial assistance of Dr. Rona M. Silva.

Disclosure statement

The research described in this article has been reviewed by the National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency and approved for publication. Approval does not signify that the contents necessarily reflect the view and the policies of the Agency nor does mention of trade names or commercial products constitute endorsement or recommendation for use.

Author contributions

PU and CWW wrote the manuscript and performed the literature search, AP contributed to the original writing and ideas for the review, AAZ, CMR, UPK, MT and HB provided data for animal models and mechanisms of COPD, KEP oversaw the organization, writing and final review.

Data availability statement

The authors confirm that the data supporting the findings of this study are available within the article and its supplementary materials https://doi.org/10.6084/m9.figshare.21354531.v1.

Supplemental data

Supplemental data for this article can be accessed online at https://doi.org/10.1080/10937404.2023.2208886.

Additional information

Funding

The preparation of this article has been facilitated through the following: National Institute for Occupational Safety and Health (NIOSH) grant U54 OH07550, National Institute of Environmental Health Sciences (NIEHS) grants U01 ES027288, P30 ES023513, and P51 OD011107, Christopher M. Royer is supported by grant K01 OD024782.