The effects of dual IQOS and cigarette smoke exposure on airway epithelial cells: implications for lung health and respiratory disease pathogenesis
Background Cigarette smoking remains a primary cause of chronic lung diseases. After a steady decline, smoking rates have recently increased especially with the introduction of newer electronic nicotine delivery devices, and it is also emerging that dual- or poly-product usage is on the rise. Additi...
| Main Authors: | , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
European Respiratory Society
2023-05-01
|
| Series: | ERJ Open Research |
| Online Access: | http://openres.ersjournals.com/content/9/3/00558-2022.full |
| _version_ | 1797689336141971456 |
|---|---|
| author | Pritam Saha Siddhi Jain Ipsita Mukherjee Samir R. Panda Amir A. Zeki V.G.M. Naidu Pawan Sharma |
| author_facet | Pritam Saha Siddhi Jain Ipsita Mukherjee Samir R. Panda Amir A. Zeki V.G.M. Naidu Pawan Sharma |
| author_sort | Pritam Saha |
| collection | DOAJ |
| description | Background
Cigarette smoking remains a primary cause of chronic lung diseases. After a steady decline, smoking rates have recently increased especially with the introduction of newer electronic nicotine delivery devices, and it is also emerging that dual- or poly-product usage is on the rise. Additionally, with the introduction of IQOS (a heated tobacco product) globally, its impact on human health needs to be investigated. In this study we tested if dual exposure (cigarette smoke (CS)+IQOS) is detrimental to lung epithelial cells when compared with CS or IQOS exposure alone.
Methods
Human airway epithelial cells (BEAS-2B) were exposed to either CS, IQOS or their dual combination (CS+IQOS) at concentrations of 0.1%, 1.0%, 2.5% and 5.0%. Cytotoxicity, oxidative stress, mitochondrial homeostasis, mitophagy and effects on epithelial–mesenchymal transition (EMT) signalling were assessed.
Results
Both CS and IQOS alone significantly induced loss of cell viability in a concentration-dependent manner which was further enhanced by dual exposure compared with IQOS alone (p<0.01). Dual exposure significantly increased oxidative stress and perturbed mitochondrial homeostasis when compared with CS or IQOS alone (p<0.05). Additionally, dual exposure induced EMT signalling as shown by increased mesenchymal (α-smooth muscle actin and N-cadherin) and decreased epithelial (E-cadherin) markers when compared with CS or IQOS alone (p<0.05).
Conclusion
Collectively, our study demonstrates that dual CS+IQOS exposure enhances pathogenic signalling mediated by oxidative stress and mitochondrial dysfunction leading to EMT activation, which is an important regulator of small airway fibrosis in obstructive lung diseases. |
| first_indexed | 2024-03-12T01:44:13Z |
| format | Article |
| id | doaj.art-447cf696da0c47c38aea1e5d5ebdaa9b |
| institution | Directory Open Access Journal |
| issn | 2312-0541 |
| language | English |
| last_indexed | 2024-03-12T01:44:13Z |
| publishDate | 2023-05-01 |
| publisher | European Respiratory Society |
| record_format | Article |
| series | ERJ Open Research |
| spelling | doaj.art-447cf696da0c47c38aea1e5d5ebdaa9b2023-09-09T13:53:54ZengEuropean Respiratory SocietyERJ Open Research2312-05412023-05-019310.1183/23120541.00558-202200558-2022The effects of dual IQOS and cigarette smoke exposure on airway epithelial cells: implications for lung health and respiratory disease pathogenesisPritam Saha0Siddhi Jain1Ipsita Mukherjee2Samir R. Panda3Amir A. Zeki4V.G.M. Naidu5Pawan Sharma6 Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research Guwahati, Guwahati, India Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research Guwahati, Guwahati, India Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research Guwahati, Guwahati, India Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research Guwahati, Guwahati, India UC Davis School of Medicine, UC Davis Lung Center and Department of Internal Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, University of California – Davis, Sacramento, CA, USA Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research Guwahati, Guwahati, India Center for Translational Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, Jane and Leonard Korman Respiratory Institute, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA Background Cigarette smoking remains a primary cause of chronic lung diseases. After a steady decline, smoking rates have recently increased especially with the introduction of newer electronic nicotine delivery devices, and it is also emerging that dual- or poly-product usage is on the rise. Additionally, with the introduction of IQOS (a heated tobacco product) globally, its impact on human health needs to be investigated. In this study we tested if dual exposure (cigarette smoke (CS)+IQOS) is detrimental to lung epithelial cells when compared with CS or IQOS exposure alone. Methods Human airway epithelial cells (BEAS-2B) were exposed to either CS, IQOS or their dual combination (CS+IQOS) at concentrations of 0.1%, 1.0%, 2.5% and 5.0%. Cytotoxicity, oxidative stress, mitochondrial homeostasis, mitophagy and effects on epithelial–mesenchymal transition (EMT) signalling were assessed. Results Both CS and IQOS alone significantly induced loss of cell viability in a concentration-dependent manner which was further enhanced by dual exposure compared with IQOS alone (p<0.01). Dual exposure significantly increased oxidative stress and perturbed mitochondrial homeostasis when compared with CS or IQOS alone (p<0.05). Additionally, dual exposure induced EMT signalling as shown by increased mesenchymal (α-smooth muscle actin and N-cadherin) and decreased epithelial (E-cadherin) markers when compared with CS or IQOS alone (p<0.05). Conclusion Collectively, our study demonstrates that dual CS+IQOS exposure enhances pathogenic signalling mediated by oxidative stress and mitochondrial dysfunction leading to EMT activation, which is an important regulator of small airway fibrosis in obstructive lung diseases.http://openres.ersjournals.com/content/9/3/00558-2022.full |
| spellingShingle | Pritam Saha Siddhi Jain Ipsita Mukherjee Samir R. Panda Amir A. Zeki V.G.M. Naidu Pawan Sharma The effects of dual IQOS and cigarette smoke exposure on airway epithelial cells: implications for lung health and respiratory disease pathogenesis ERJ Open Research |
| title | The effects of dual IQOS and cigarette smoke exposure on airway epithelial cells: implications for lung health and respiratory disease pathogenesis |
| title_full | The effects of dual IQOS and cigarette smoke exposure on airway epithelial cells: implications for lung health and respiratory disease pathogenesis |
| title_fullStr | The effects of dual IQOS and cigarette smoke exposure on airway epithelial cells: implications for lung health and respiratory disease pathogenesis |
| title_full_unstemmed | The effects of dual IQOS and cigarette smoke exposure on airway epithelial cells: implications for lung health and respiratory disease pathogenesis |
| title_short | The effects of dual IQOS and cigarette smoke exposure on airway epithelial cells: implications for lung health and respiratory disease pathogenesis |
| title_sort | effects of dual iqos and cigarette smoke exposure on airway epithelial cells implications for lung health and respiratory disease pathogenesis |
| url | http://openres.ersjournals.com/content/9/3/00558-2022.full |
| work_keys_str_mv | AT pritamsaha theeffectsofdualiqosandcigarettesmokeexposureonairwayepithelialcellsimplicationsforlunghealthandrespiratorydiseasepathogenesis AT siddhijain theeffectsofdualiqosandcigarettesmokeexposureonairwayepithelialcellsimplicationsforlunghealthandrespiratorydiseasepathogenesis AT ipsitamukherjee theeffectsofdualiqosandcigarettesmokeexposureonairwayepithelialcellsimplicationsforlunghealthandrespiratorydiseasepathogenesis AT samirrpanda theeffectsofdualiqosandcigarettesmokeexposureonairwayepithelialcellsimplicationsforlunghealthandrespiratorydiseasepathogenesis AT amirazeki theeffectsofdualiqosandcigarettesmokeexposureonairwayepithelialcellsimplicationsforlunghealthandrespiratorydiseasepathogenesis AT vgmnaidu theeffectsofdualiqosandcigarettesmokeexposureonairwayepithelialcellsimplicationsforlunghealthandrespiratorydiseasepathogenesis AT pawansharma theeffectsofdualiqosandcigarettesmokeexposureonairwayepithelialcellsimplicationsforlunghealthandrespiratorydiseasepathogenesis AT pritamsaha effectsofdualiqosandcigarettesmokeexposureonairwayepithelialcellsimplicationsforlunghealthandrespiratorydiseasepathogenesis AT siddhijain effectsofdualiqosandcigarettesmokeexposureonairwayepithelialcellsimplicationsforlunghealthandrespiratorydiseasepathogenesis AT ipsitamukherjee effectsofdualiqosandcigarettesmokeexposureonairwayepithelialcellsimplicationsforlunghealthandrespiratorydiseasepathogenesis AT samirrpanda effectsofdualiqosandcigarettesmokeexposureonairwayepithelialcellsimplicationsforlunghealthandrespiratorydiseasepathogenesis AT amirazeki effectsofdualiqosandcigarettesmokeexposureonairwayepithelialcellsimplicationsforlunghealthandrespiratorydiseasepathogenesis AT vgmnaidu effectsofdualiqosandcigarettesmokeexposureonairwayepithelialcellsimplicationsforlunghealthandrespiratorydiseasepathogenesis AT pawansharma effectsofdualiqosandcigarettesmokeexposureonairwayepithelialcellsimplicationsforlunghealthandrespiratorydiseasepathogenesis |