Tags

Type your tag names separated by a space and hit enter

Fighting the Host Reaction to SARS-COv-2 in Critically Ill Patients: The Possible Contribution of Off-Label Drugs.
Front Immunol. 2020; 11:1201.FI

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-COv-2) is the etiologic agent of the 2019 coronavirus disease (COVID19). The majority of infected people presents flu like symptoms and among them 15-20% develops a severe interstitial pneumonitis (IP) that may eventually evolve in acute respiratory distress syndrome (ARDS). IP is caused by the viral glycoprotein spike (S) binding to the angiotensin converting enzyme 2 (ACE2) expressed on the surface of alveolar pneumocytes. The virus is recognized by the "pattern recognition receptors" (PRR) of the immune cells that release cytokines activating more immune cells that produce a large number of pro-inflammatory cytokines, tissue factors and vasoactive peptides. Affected patients might develop the "cytokine storm syndrome," a fulminant and fatal hypercytokinaemia with multiorgan failure. In patients infected by SARS-COv-2 increase in T-helper 2 (TH2) cytokines (IL-4 and IL10) are reported in addition to the T-helper 1 (TH1) cytokines (IL1B, IFNγ, IP10, and MCP1) previously detected in other coronavirus infections. Cytokines and other molecules involved in immune response and inflammation are conceivable therapeutic targets for IP and ARDS, improving symptoms and decreasing intensive care unit admissions. To this aim off label drugs may be used taking into consideration the window timing for immunosuppressive drugs in virus infected patients. Some off label therapeutic options and preclinical evidence drugs are herein considered.

Authors+Show Affiliations

Functional Genomics, Istituto Nazionale per lo Studio e la Cura dei Tumori, "Fondazione G. Pascale" - IRCCS, Naples, Italy.Department of Advanced Biomedical Sciences, School of Medicine, University Federico II, Naples, Italy.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

32574268

Citation

Scala, Stefania, and Roberto Pacelli. "Fighting the Host Reaction to SARS-COv-2 in Critically Ill Patients: the Possible Contribution of Off-Label Drugs." Frontiers in Immunology, vol. 11, 2020, p. 1201.
Scala S, Pacelli R. Fighting the Host Reaction to SARS-COv-2 in Critically Ill Patients: The Possible Contribution of Off-Label Drugs. Front Immunol. 2020;11:1201.
Scala, S., & Pacelli, R. (2020). Fighting the Host Reaction to SARS-COv-2 in Critically Ill Patients: The Possible Contribution of Off-Label Drugs. Frontiers in Immunology, 11, 1201. https://doi.org/10.3389/fimmu.2020.01201
Scala S, Pacelli R. Fighting the Host Reaction to SARS-COv-2 in Critically Ill Patients: the Possible Contribution of Off-Label Drugs. Front Immunol. 2020;11:1201. PubMed PMID: 32574268.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fighting the Host Reaction to SARS-COv-2 in Critically Ill Patients: The Possible Contribution of Off-Label Drugs. AU - Scala,Stefania, AU - Pacelli,Roberto, Y1 - 2020/05/27/ PY - 2020/03/31/received PY - 2020/05/14/accepted PY - 2020/6/24/entrez PY - 2020/6/24/pubmed PY - 2020/7/11/medline KW - cytokine KW - inflammation KW - interstitial pneumonia KW - macrophages KW - offlabel drug use SP - 1201 EP - 1201 JF - Frontiers in immunology JO - Front Immunol VL - 11 N2 - The severe acute respiratory syndrome coronavirus 2 (SARS-COv-2) is the etiologic agent of the 2019 coronavirus disease (COVID19). The majority of infected people presents flu like symptoms and among them 15-20% develops a severe interstitial pneumonitis (IP) that may eventually evolve in acute respiratory distress syndrome (ARDS). IP is caused by the viral glycoprotein spike (S) binding to the angiotensin converting enzyme 2 (ACE2) expressed on the surface of alveolar pneumocytes. The virus is recognized by the "pattern recognition receptors" (PRR) of the immune cells that release cytokines activating more immune cells that produce a large number of pro-inflammatory cytokines, tissue factors and vasoactive peptides. Affected patients might develop the "cytokine storm syndrome," a fulminant and fatal hypercytokinaemia with multiorgan failure. In patients infected by SARS-COv-2 increase in T-helper 2 (TH2) cytokines (IL-4 and IL10) are reported in addition to the T-helper 1 (TH1) cytokines (IL1B, IFNγ, IP10, and MCP1) previously detected in other coronavirus infections. Cytokines and other molecules involved in immune response and inflammation are conceivable therapeutic targets for IP and ARDS, improving symptoms and decreasing intensive care unit admissions. To this aim off label drugs may be used taking into consideration the window timing for immunosuppressive drugs in virus infected patients. Some off label therapeutic options and preclinical evidence drugs are herein considered. SN - 1664-3224 UR - https://www.unboundmedicine.com/medline/citation/32574268/Fighting_the_Host_Reaction_to_SARS-COv-2_in_Critically_Ill_Patients:_The_Possible_Contribution_of_Off-Label_Drugs L2 - https://doi.org/10.3389/fimmu.2020.01201 DB - PRIME DP - Unbound Medicine ER -