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.
Highlights
SARS-CoV-2 is a new coronavirus that originated in Wuhan (Hubei Province, China) in December 2019, and it has already developed into a pandemic with worldwide spread [1]
Among different cytokines increased in such exacerbated response [5], Interleukin-6 (IL-6) in serum is mainly expected to predict the severity of SARS-CoV2 pneumonia, as suppression of pro-inflammatory IL-6 have been shown to have a therapeutic effect in many inflammatory diseases, including viral infections [6]
Smoking is significantly associated with MERS-CoV [16], and there is no clear evidence for SARS-CoV-2 [17]
Summary
SARS-CoV-2 is a new coronavirus that originated in Wuhan (Hubei Province, China) in December 2019, and it has already developed into a pandemic with worldwide spread [1]. SARS-CoV-2 has been shown to activate both the innate and adaptive immune system in the alveolar tissue, inducing the release of many cytokines and subsequent cytokine release syndrome [7] During this response, levels of pro-inflammatory cytokines (including TNFa, interleukin (IL)1b, IL-6, and IL-8) are increased [5], which is an important cause of death [8]. In other inflammatory diseases, such as ulcerative Colitis (UC), smoking or treatment with nicotine has demonstrated to significantly decrease the risk of developing the disease [14] In this scenario, we hypothesize that nicotine could ameliorate the cytokine storm and severe related inflammatory response through a7nAChR-mediated cholinergic anti-inflammatory pathway. Nicotine is an accessible, existing, and approved treatment, with described side effects, that could likely reduce the rising mortality in the short term It is well-stablished that smokers have a significantly increased risk of chronic respiratory disease and acute respiratory infections.
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