| Literature DB >> 33362782 |
Ralf Kircheis1, Emanuel Haasbach2, Daniel Lueftenegger1, Willm T Heyken1, Matthias Ocker3, Oliver Planz2.
Abstract
Patients infected with SARS-CoV-2 show a wide spectrum of clinical manifestations ranging from mild febrile illness and cough up to acute respiratory distress syndrome, multiple organ failure, and death. Data from patients with severe clinical manifestations compared to patients with mild symptoms indicate that highly dysregulated exuberant inflammatory responses correlate with severity of disease and lethality. Epithelial-immune cell interactions and elevated cytokine and chemokine levels, i.e. cytokine storm, seem to play a central role in severity and lethality in COVID-19. The present perspective places a central cellular pro-inflammatory signal pathway, NF-κB, in the context of recently published data for COVID-19 and provides a hypothesis for a therapeutic approach aiming at the simultaneous inhibition of whole cascades of pro-inflammatory cytokines and chemokines. The simultaneous inhibition of multiple cytokines/chemokines is expected to have much higher therapeutic potential as compared to single target approaches to prevent cascade (i.e. redundant, triggering, amplifying, and synergistic) effects of multiple induced cytokines and chemokines in critical stage COVID-19 patients.Entities:
Keywords: COVID-19; NF-KappaB; NSAID; SARS-CoV-2 (2019-nCoV); chemokines; cytokine storm; cytokines; proteasome inhibitor
Year: 2020 PMID: 33362782 PMCID: PMC7759159 DOI: 10.3389/fimmu.2020.598444
Source DB: PubMed Journal: Front Immunol ISSN: 1664-3224 Impact factor: 7.561