Literature DB >> 33379366

Nicotine Changes Airway Epithelial Phenotype and May Increase the SARS-COV-2 Infection Severity.

Leonardo Lupacchini1, Fabrizio Maggi2, Carlo Tomino3, Chiara De Dominicis1, Cristiana Mollinari4,5, Massimo Fini3, Stefano Bonassi6,7, Daniela Merlo5, Patrizia Russo6,7.   

Abstract

(1) Background: Nicotine is implicated in the SARS-COV-2 infection through activation of the α7-nAChR and over-expression of ACE2. Our objective was to clarify the role of nicotine in SARS-CoV-2 infection exploring its molecular and cellular activity. (2)
Methods: HBEpC or si-mRNA-α7-HBEpC were treated for 1 h, 48 h or continuously with 10-7 M nicotine, a concentration mimicking human exposure to a cigarette. Cell viability and proliferation were evaluated by trypan blue dye exclusion and cell counting, migration by cell migration assay, senescence by SA-β-Gal activity, and anchorage-independent growth by cloning in soft agar. Expression of Ki67, p53/phospho-p53, VEGF, EGFR/pEGFR, phospho-p38, intracellular Ca2+, ATP and EMT were evaluated by ELISA and/or Western blotting. (3)
Results: nicotine induced through α7-nAChR (i) increase in cell viability, (ii) cell proliferation, (iii) Ki67 over-expression, (iv) phospho-p38 up-regulation, (v) EGFR/pEGFR over-expression, (vi) increase in basal Ca2+ concentration, (vii) reduction of ATP production, (viii) decreased level of p53/phospho-p53, (ix) delayed senescence, (x) VEGF increase, (xi) EMT and consequent (xii) enhanced migration, and (xiii) ability to grow independently of the substrate. (4) Conclusions: Based on our results and on evidence showing that nicotine potentiates viral infection, it is likely that nicotine is involved in SARS-CoV-2 infection and severity.

Entities:  

Keywords:  EMT; SARS-CoV-2; cell proliferation; mitochondrial dysfunction; nAChR; nicotine

Year:  2020        PMID: 33379366     DOI: 10.3390/molecules26010101

Source DB:  PubMed          Journal:  Molecules        ISSN: 1420-3049            Impact factor:   4.411


  6 in total

Review 1.  Tryptophan Metabolites and Aryl Hydrocarbon Receptor in Severe Acute Respiratory Syndrome, Coronavirus-2 (SARS-CoV-2) Pathophysiology.

Authors:  George Anderson; Annalucia Carbone; Gianluigi Mazzoccoli
Journal:  Int J Mol Sci       Date:  2021-02-05       Impact factor: 5.923

2.  Nicotinic receptors as SARS-CoV-2 spike co-receptors?

Authors:  Valérian Dormoy; Jeanne-Marie Perotin; Philippe Gosset; Uwe Maskos; Myriam Polette; Gaëtan Deslée
Journal:  Med Hypotheses       Date:  2021-12-14       Impact factor: 1.538

3.  Nicotine has no significant cytoprotective activity against SARS-CoV-2 infection.

Authors:  Fang Zheng; Elena Lian; Gaby Ramirez; Carley McAlister; Shuo Zhou; Wen Zhang; Chunming Liu; Rushika Perera; Chang-Guo Zhan
Journal:  PLoS One       Date:  2022-08-18       Impact factor: 3.752

4.  Nicotine in Combination with SARS-CoV-2 Affects Cells Viability, Inflammatory Response and Ultrastructural Integrity.

Authors:  Luigi Sansone; Antonio de Iure; Mario Cristina; Manuel Belli; Laura Vitiello; Federica Marcolongo; Alfredo Rosellini; Lisa Macera; Pietro Giorgio Spezia; Carlo Tomino; Stefano Bonassi; Matteo A Russo; Fabrizio Maggi; Patrizia Russo
Journal:  Int J Mol Sci       Date:  2022-08-22       Impact factor: 6.208

5.  Lower Gene Expression of Angiotensin Converting Enzyme 2 Receptor in Lung Tissues of Smokers with COVID-19 Pneumonia.

Authors:  Francesca Lunardi; Francesco Fortarezza; Luca Vedovelli; Federica Pezzuto; Annalisa Boscolo; Marco Rossato; Roberto Vettor; Anna Maria Cattelan; Claudia Del Vecchio; Andrea Crisanti; Paolo Navalesi; Dario Gregori; Fiorella Calabrese
Journal:  Biomolecules       Date:  2021-05-26

Review 6.  COVID-19 in Joint Ageing and Osteoarthritis: Current Status and Perspectives.

Authors:  Marianne Lauwers; Manting Au; Shuofeng Yuan; Chunyi Wen
Journal:  Int J Mol Sci       Date:  2022-01-10       Impact factor: 5.923

  6 in total

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