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*Acknowledgement: This research was supported by the grant from Ministry of Science and Technology of China under a contract from the International Science & Technology Cooperation Program Foundation Nr.1019 and the National Natural Science Foundation of China (Grant No. 81500859). | *Acknowledgement: This research was supported by the grant from Ministry of Science and Technology of China under a contract from the International Science & Technology Cooperation Program Foundation Nr.1019 and the National Natural Science Foundation of China (Grant No. 81500859). | ||
*Citation: An, N., Holl, J., Wang, X., Rausch, M. A., Andrukhov, O., & Rausch-Fan, X. (2021). Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study. International Journal of Environmental Research and Public Health, 18(2), 483. https://doi.org/10.3390/ijerph18020483 | *Citation: An, N., Holl, J., Wang, X., Rausch, M. A., Andrukhov, O., & Rausch-Fan, X. (2021). Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study. International Journal of Environmental Research and Public Health, 18(2), 483. https://doi.org/10.3390/ijerph18020483 | ||
===2020 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7704168/ Does Nicotine Prevent Cytokine Storms in COVID-19?]=== | |||
*Case study of one individual | |||
*Nicotine, an α7-nACh receptor agonist, may boost the cholinergic anti-inflammatory pathway and hinder the uncontrolled overproduction of pro-inflammatory cytokines triggered by the SARS-CoV-2 virus, which is understood to be the main pathway to poor outcomes and death in severe COVID-19. | |||
*In the absence of any effective treatment for COVID-19, further research as to whether nicotine replacement offers protection against severe SAR-CoV-2 infection in smokers is clearly essential. If the mechanisms through which nicotine may interact with the virus remain speculative, the effects of route of administration, duration, dosing and frequency of use of nicotine on any such interaction are unknown. Should NRT be found to be of help in the management of COVID-19, it would be yet another strong reason to persuade smokers to switch to NRT and ultimately quit smoking. | |||
*Citation: Dratcu L, Boland X. Does Nicotine Prevent Cytokine Storms in COVID-19? Cureus. 2020 Oct 28;12(10):e11220. doi: 10.7759/cureus.11220. PMID: 33269148; PMCID: PMC7704168. | |||
===2020 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7300218/ Cytokine Release Syndrome (CRS) and Nicotine in COVID-19 Patients: Trying to Calm the Storm]=== | |||
*Abstract: "SARS-CoV-2 is a new coronavirus that has caused a worldwide pandemic. It causes severe acute respiratory syndrome (COVID-19), which is fatal in many cases, and is characterized by a cytokine release syndrome (CRS). Great efforts are currently being made to block the signal transduction pathway of pro-inflammatory cytokines in order to control this “cytokine storm” and rescue severely affected patients. Consequently, possible treatments for cytokine-mediated hyperinflammation, preferably within approved safe therapies, are urgently being researched to reduce rising mortality. One approach to inhibit proinflammatory cytokine release is to activate the cholinergic anti-inflammatory pathway through nicotinic acetylcholine receptors (α7nAchR). Nicotine, an exogenous α7nAchR agonist, is clinically used in ulcerative colitis to counteract inflammation. We have found epidemiological evidence, based on recent clinical SARS-CoV-2 studies in China, that suggest that smokers are statistically less likely to be hospitalized. In conclusion, our hypothesis proposes that nicotine could constitute a novel potential CRS therapy in severe SARS-CoV-2 patients." | |||
*Citation: Gonzalez-Rubio J, Navarro-Lopez C, Lopez-Najera E, Lopez-Najera A, Jimenez-Diaz L, Navarro-Lopez JD, Najera A. Cytokine Release Syndrome (CRS) and Nicotine in COVID-19 Patients: Trying to Calm the Storm. Front Immunol. 2020 Jun 11;11:1359. doi: 10.3389/fimmu.2020.01359. PMID: 32595653; PMCID: PMC7300218. | |||
===2016 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760232/ Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis]=== | ===2016 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760232/ Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis]=== | ||
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