Synergistic Detrimental Effects of Cigarette Smoke, Alcohol, and SARS-CoV-2 in COPD Bronchial Epithelial Cells
Abenaya Muralidharan,
Christopher D. Bauer,
Dawn M. Katafiasz,
Heather M. Strah,
Aleem Siddique,
St Patrick Reid,
Kristina L. Bailey,
Todd A. Wyatt
Affiliations
Abenaya Muralidharan
Department of Pathology and Microbiology, College of Medicine, The University of Nebraska Medical Center, Omaha, NE 68198, USA
Christopher D. Bauer
Pulmonary, Critical Care, and Sleep Medicine Division, Department of Internal Medicine, College of Medicine, the University of Nebraska Medical Center, Omaha, NE 68198, USA
Dawn M. Katafiasz
Pulmonary, Critical Care, and Sleep Medicine Division, Department of Internal Medicine, College of Medicine, the University of Nebraska Medical Center, Omaha, NE 68198, USA
Heather M. Strah
Pulmonary, Critical Care, and Sleep Medicine Division, Department of Internal Medicine, College of Medicine, the University of Nebraska Medical Center, Omaha, NE 68198, USA
Aleem Siddique
Department of Surgery, College of Medicine, the University of Nebraska Medical Center, Omaha, NE 68198, USA
St Patrick Reid
Department of Pathology and Microbiology, College of Medicine, The University of Nebraska Medical Center, Omaha, NE 68198, USA
Kristina L. Bailey
Pulmonary, Critical Care, and Sleep Medicine Division, Department of Internal Medicine, College of Medicine, the University of Nebraska Medical Center, Omaha, NE 68198, USA
Todd A. Wyatt
Pulmonary, Critical Care, and Sleep Medicine Division, Department of Internal Medicine, College of Medicine, the University of Nebraska Medical Center, Omaha, NE 68198, USA
Lung conditions such as COPD, as well as risk factors such as alcohol misuse and cigarette smoking, can exacerbate COVID-19 disease severity. Synergistically, these risk factors can have a significant impact on immunity against pathogens. Here, we studied the effect of a short exposure to alcohol and/or cigarette smoke extract (CSE) in vitro on acute SARS-CoV-2 infection of ciliated human bronchial epithelial cells (HBECs) collected from healthy and COPD donors. We observed an increase in viral titer in CSE- or alcohol-treated COPD HBECs compared to untreated COPD HBECs. Furthermore, we treated healthy HBECs accompanied by enhanced lactate dehydrogenase activity, indicating exacerbated injury. Finally, IL-8 secretion was elevated due to the synergistic damage mediated by alcohol, CSE, and SARS-CoV-2 in COPD HBECs. Together, our data suggest that, with pre-existing COPD, short exposure to alcohol or CSE is sufficient to exacerbate SARS-CoV-2 infection and associated injury, impairing lung defences.
