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Can Beta-2-Adrenergic Pathway Be a New Target to Combat SARS-CoV-2 Hyperinflammatory Syndrome?-Lessons Learned From Cancer.
Front Immunol. 2020; 11:588724.FI

Abstract

SARS-CoV-2 infection is a new threat to global public health in the 21st century (2020), which has now rapidly spread around the globe causing severe pneumonia often linked to Acute Respiratory Distress Syndrome (ARDS) and hyperinflammatory syndrome. SARS-CoV-2 is highly contagious through saliva droplets. The structural analysis suggests that the virus enters human cells through the ligation of the spike protein to angiotensin-converting enzyme 2 (ACE2). The progression of Covid-19 has been divided into three main stages: stage I-viral response, stage II-pulmonary phase, and stage III-hyperinflammation phase. Once the patients enter stage III, it will likely need ventilation and it becomes difficult to manage. Thus, it will be of paramount importance to find therapies to prevent or slow down the progression of the disease toward stage III. The key event leading to hyperinflammation seems to be the activation of Th-17 immunity response and Cytokine storm. B2-adrenergic receptors (B2ARs) are expressed on airways and on all the immune cells such as macrophages, dendritic cells, B and T lymphocytes. Blocking (B2AR) has been proven, also in clinical settings, to reduce Th-17 response and negatively modulate inflammatory cytokines including IL-6 while increasing IFNγ. Non-selective beta-blockers are currently used to treat several diseases and have been proven to reduce stress-induced inflammation and reduce anxiety. For these reasons, we speculate that targeting B2AR in the early phase of Covid-19 might be beneficial to prevent hyperinflammation.

Authors+Show Affiliations

Animal Facility, Istituto Nazionale Tumori, Istituto Di Ricovero e Cura a Carattere Scientifico "Fondazione G. Pascale", Naples, Italy.Centre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, Australia.Animal Facility, Istituto Nazionale Tumori, Istituto Di Ricovero e Cura a Carattere Scientifico "Fondazione G. Pascale", Naples, Italy.Division of Cardiology, Istituto Nazionale Tumori, Istituto Di Ricovero e Cura a Carattere Scientifico (IRCCS) "Fondazione G. Pascale", Naples, Italy.Section of Histology, Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy.Scientific Directorate, Istituto Nazionale Tumori, IRCCS "Fondazione G. Pascale", Naples, Italy.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

33117402

Citation

Barbieri, Antonio, et al. "Can Beta-2-Adrenergic Pathway Be a New Target to Combat SARS-CoV-2 Hyperinflammatory Syndrome?-Lessons Learned From Cancer." Frontiers in Immunology, vol. 11, 2020, p. 588724.
Barbieri A, Robinson N, Palma G, et al. Can Beta-2-Adrenergic Pathway Be a New Target to Combat SARS-CoV-2 Hyperinflammatory Syndrome?-Lessons Learned From Cancer. Front Immunol. 2020;11:588724.
Barbieri, A., Robinson, N., Palma, G., Maurea, N., Desiderio, V., & Botti, G. (2020). Can Beta-2-Adrenergic Pathway Be a New Target to Combat SARS-CoV-2 Hyperinflammatory Syndrome?-Lessons Learned From Cancer. Frontiers in Immunology, 11, 588724. https://doi.org/10.3389/fimmu.2020.588724
Barbieri A, et al. Can Beta-2-Adrenergic Pathway Be a New Target to Combat SARS-CoV-2 Hyperinflammatory Syndrome?-Lessons Learned From Cancer. Front Immunol. 2020;11:588724. PubMed PMID: 33117402.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Can Beta-2-Adrenergic Pathway Be a New Target to Combat SARS-CoV-2 Hyperinflammatory Syndrome?-Lessons Learned From Cancer. AU - Barbieri,Antonio, AU - Robinson,Nirmal, AU - Palma,Giuseppe, AU - Maurea,Nicola, AU - Desiderio,Vincenzo, AU - Botti,Gerardo, Y1 - 2020/09/30/ PY - 2020/07/29/received PY - 2020/09/17/accepted PY - 2020/10/29/entrez PY - 2020/10/30/pubmed PY - 2020/11/11/medline KW - Beta adrenergic receptors KW - COVID-19 KW - Cytokine storm KW - SARS-CoV2 KW - beta-blockers KW - hyperinflammation KW - immune response SP - 588724 EP - 588724 JF - Frontiers in immunology JO - Front Immunol VL - 11 N2 - SARS-CoV-2 infection is a new threat to global public health in the 21st century (2020), which has now rapidly spread around the globe causing severe pneumonia often linked to Acute Respiratory Distress Syndrome (ARDS) and hyperinflammatory syndrome. SARS-CoV-2 is highly contagious through saliva droplets. The structural analysis suggests that the virus enters human cells through the ligation of the spike protein to angiotensin-converting enzyme 2 (ACE2). The progression of Covid-19 has been divided into three main stages: stage I-viral response, stage II-pulmonary phase, and stage III-hyperinflammation phase. Once the patients enter stage III, it will likely need ventilation and it becomes difficult to manage. Thus, it will be of paramount importance to find therapies to prevent or slow down the progression of the disease toward stage III. The key event leading to hyperinflammation seems to be the activation of Th-17 immunity response and Cytokine storm. B2-adrenergic receptors (B2ARs) are expressed on airways and on all the immune cells such as macrophages, dendritic cells, B and T lymphocytes. Blocking (B2AR) has been proven, also in clinical settings, to reduce Th-17 response and negatively modulate inflammatory cytokines including IL-6 while increasing IFNγ. Non-selective beta-blockers are currently used to treat several diseases and have been proven to reduce stress-induced inflammation and reduce anxiety. For these reasons, we speculate that targeting B2AR in the early phase of Covid-19 might be beneficial to prevent hyperinflammation. SN - 1664-3224 UR - https://www.unboundmedicine.com/medline/citation/33117402/Can_Beta_2_Adrenergic_Pathway_Be_a_New_Target_to_Combat_SARS_CoV_2_Hyperinflammatory_Syndrome_Lessons_Learned_From_Cancer_ L2 - https://doi.org/10.3389/fimmu.2020.588724 DB - PRIME DP - Unbound Medicine ER -