Sunday, May 03, 2020

Time To Pick Up A Pack Of Nicorette


sciencedirect |   Nicotine could act as a competitive agonist for the nAChRs that could restore the compromised function of the nicotinic cholinergic system. This may be feasible through repurposing already approved (for other indications) pharmaceutical nicotine products such as nicotine patches for use by non-smokers, or even by using these products as already indicated (i.e. as smoking substitutes) among current smokers. These products are available over-the-counter in most countries. They have been administered therapeutically in non-smokers for neurological conditions and inflammatory bowel disease for larger periods than would be needed for COVID-19 [[81], [82], [83]]. No abuse liability was observed in non-smokers despite being administerd for several weeks [82,83]. Besides gums and patches, nicotine can be administered though inhalation, with the use of a nebulizer or other aerosol systems, if necessary. Nicotine administration could be added on top of antiviral or other therapeutic options for COVID-19. By restoring and re-activating the cholinergic anti-inflammatory pathway, a more universal suppression of the cytokine storm could probably be achieved compared to administering inhibitors of a single cytokine. The potential need to provide pharmaceutical nicotine products to smokers and users of other nicotine products who experience abrupt withdrawal symptoms of nicotine when hospitalized for COVID-19 or aim to follow medical advice to quit smoking, should also be examined. Additionally, if the hypothesis about the beneficial effects of nicotine is valid, smokers who quit nicotine use when hospitalized will be deprived from these benefits. In France, the Addiction Prevention Network (RESPADD) officially recommends the use of nicotine replacement therapies for smokers when hospitalized for any illness [84]. Clinical trials will dictate future approaches and the role of nicotine in COVID-19, while further experimental studies should examine the affinity of the virus to nAChRs.

Conclusions
In conclusion, we noticed that most of the clinical characteristics of severe COVID-19 could be explained by dysregulation of the cholinergic anti-inflammatory system. The observation that patients eventually develop cytokine storm which results in rapid clinical deterioration, led to the development of a hypothesis about the series of events associated with adverse outcomes in COVID-19 (Fig. 2).


Once someone is infected with SARS-CoV-2, the immune system is mobilized. As the virus replicates, cell and viral debris or virions may interact with the nAChRs blocking the action of the cholinergic anti-inflammatory pathway. If the initial immune response is not enough to combat the viral invasion at an early stage, the extensive and prolonged replication of the virus will eventually block a large part the cholinergic anti-inflammatory pathway seriously compromising its ability to control and regulate the immune response. The uncontrolled action of pro-inflammatory cytokines will result in the development of cytokine storm, with acute lung injury leading to ARDS, coagulation disturbances and multiorgan failure. Based on this hypothesis, COVID-19 appears to eventually become a disease of the nicotinic cholinergic system. Nicotine could maintain or restore the function of the cholinergic anti-inflammatory system and thus control the release and activity of pro-inflammatory cytokines. This could prevent or suppress the cytokine storm. This hypothesis needs to be examined in the laboratory and the clinical setting.

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