K. Farsalinos, A. Angelopoulou, Nikos Alexandris, K. Poulas
European Respiratory Journal, 2020
We have read with great interest the paper by Leung et al. [1] published in the European Respiratory Journal, the correspondence by Russo et al. [2], and also the subsequent comment by the first group [3]. Both research teams are reporting increased angiotensin-converting enzyme 2 (ACE-2) expression in airways of current smokers and those with COPD, with important implications for coronavirus disease 2019 (COVID-19) patients. Since ACE-2 has been shown to be the main receptor utilised by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to enter the host cells [2], the authors conclude that nicotine is a risk factor for COVID-19. Russo et al. [2] have shown that nicotine upregulates ACE-2 through α7-nAChRs which are present in neuronal and non-neuronal cells. Leung et al. [3] provided further evidence in support of this hypothesis and propose the repurposing of α7-nAChR antagonists for the pandemic (e.g. methyllycaconitine, α-conotoxin), expecting that such treatment will alter ACE-2 expression and prevent SARS-CoV-2 entry. The prevalence of smoking among hospitalised COVID-19 patients is low. COVID-19 manifestations could be linked to impairment of the cholinergic anti-inflammatory pathway. Nicotinic cholinergic agonists should be examined as potential therapeutic options. https://bit.ly/2zfUZ1S
Cited by 34 publications.
Field of study: Medicine