Nicotine Impairs the Response of Lung Epithelial Cells to IL-22
Smoking is a major risk factor for pulmonary diseases that include chronic obstructive pulmonary diseases (COPD) and cancer. Nicotine is the toxic and addictive component of tobacco products, like cigarettes, that negatively affects the immune system. Here, we examined the effect of nicotine on the...
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| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2020-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2020/6705428 |
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| _version_ | 1832566141569990656 |
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| author | Hannah My-Hanh Nguyen Jaclene Amber Torres Sudhanshu Agrawal Anshu Agrawal |
| author_facet | Hannah My-Hanh Nguyen Jaclene Amber Torres Sudhanshu Agrawal Anshu Agrawal |
| author_sort | Hannah My-Hanh Nguyen |
| collection | DOAJ |
| description | Smoking is a major risk factor for pulmonary diseases that include chronic obstructive pulmonary diseases (COPD) and cancer. Nicotine is the toxic and addictive component of tobacco products, like cigarettes, that negatively affects the immune system. Here, we examined the effect of nicotine on the IL-22 pathway that protects lung function by increasing transepithelial resistance and epithelial cell regeneration and repair. Our results indicate that exposure to nicotine impairs the regenerative capacity of primary bronchial epithelial cells in scratch assays. IL-22 at 100 ng/ml significantly improved wound healing in epithelial cells; however, the exposure to nicotine hampered the IL-22-mediated effect of wound healing. Investigation into the mechanisms showed that IL-22 receptor, IL-22Rα1, was downregulated in the presence of nicotine as determined by q-PCR and flow cytometry. We also investigated the effect of nicotine on IL-22 production by T cells. Results indicate that nicotine inhibited the secretion of IL-22 from T cells in response to aryl hydrocarbon receptor (AHR) ligand, FICZ. Altogether, the data suggests that nicotine negatively influences the IL-22-IL-22R axis. This impairment may contribute to the nicotine-mediated detrimental effects on lung function. |
| format | Article |
| id | doaj-art-7dc4fb40e4ac40108b31e2336bb71cd4 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2020-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-7dc4fb40e4ac40108b31e2336bb71cd42025-02-03T01:05:03ZengWileyMediators of Inflammation0962-93511466-18612020-01-01202010.1155/2020/67054286705428Nicotine Impairs the Response of Lung Epithelial Cells to IL-22Hannah My-Hanh Nguyen0Jaclene Amber Torres1Sudhanshu Agrawal2Anshu Agrawal3Division of Basic and Clinical Immunology, Department of Medicine, University of California, Irvine, Irvine, CA 92697, USADivision of Basic and Clinical Immunology, Department of Medicine, University of California, Irvine, Irvine, CA 92697, USADivision of Basic and Clinical Immunology, Department of Medicine, University of California, Irvine, Irvine, CA 92697, USADivision of Basic and Clinical Immunology, Department of Medicine, University of California, Irvine, Irvine, CA 92697, USASmoking is a major risk factor for pulmonary diseases that include chronic obstructive pulmonary diseases (COPD) and cancer. Nicotine is the toxic and addictive component of tobacco products, like cigarettes, that negatively affects the immune system. Here, we examined the effect of nicotine on the IL-22 pathway that protects lung function by increasing transepithelial resistance and epithelial cell regeneration and repair. Our results indicate that exposure to nicotine impairs the regenerative capacity of primary bronchial epithelial cells in scratch assays. IL-22 at 100 ng/ml significantly improved wound healing in epithelial cells; however, the exposure to nicotine hampered the IL-22-mediated effect of wound healing. Investigation into the mechanisms showed that IL-22 receptor, IL-22Rα1, was downregulated in the presence of nicotine as determined by q-PCR and flow cytometry. We also investigated the effect of nicotine on IL-22 production by T cells. Results indicate that nicotine inhibited the secretion of IL-22 from T cells in response to aryl hydrocarbon receptor (AHR) ligand, FICZ. Altogether, the data suggests that nicotine negatively influences the IL-22-IL-22R axis. This impairment may contribute to the nicotine-mediated detrimental effects on lung function.http://dx.doi.org/10.1155/2020/6705428 |
| spellingShingle | Hannah My-Hanh Nguyen Jaclene Amber Torres Sudhanshu Agrawal Anshu Agrawal Nicotine Impairs the Response of Lung Epithelial Cells to IL-22 Mediators of Inflammation |
| title | Nicotine Impairs the Response of Lung Epithelial Cells to IL-22 |
| title_full | Nicotine Impairs the Response of Lung Epithelial Cells to IL-22 |
| title_fullStr | Nicotine Impairs the Response of Lung Epithelial Cells to IL-22 |
| title_full_unstemmed | Nicotine Impairs the Response of Lung Epithelial Cells to IL-22 |
| title_short | Nicotine Impairs the Response of Lung Epithelial Cells to IL-22 |
| title_sort | nicotine impairs the response of lung epithelial cells to il 22 |
| url | http://dx.doi.org/10.1155/2020/6705428 |
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