Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32773102
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Devilishly radical NETwork in COVID-19: Oxidative stress, neutrophil
extracellular traps (NETs), and T cell suppression
#MMPMID32773102
Schönrich G
; Raftery MJ
; Samstag Y
Adv Biol Regul
2020[Aug]; 77
(?): 100741
PMID32773102
show ga
Pandemic coronavirus disease 2019 (COVID-19) is caused by severe acute
respiratory syndrome coronavirus 2 (SARS-CoV-2) and poses an unprecedented
challenge to healthcare systems due to the lack of a vaccine and specific
treatment options. Accordingly, there is an urgent need to understand precisely
the pathogenic mechanisms underlying this multifaceted disease. There is
increasing evidence that the immune system reacts insufficiently to SARS-CoV-2
and thus contributes to organ damage and to lethality. In this review, we suggest
that the overwhelming production of reactive oxygen species (ROS) resulting in
oxidative stress is a major cause of local or systemic tissue damage that leads
to severe COVID-19. It increases the formation of neutrophil extracellular traps
(NETs) and suppresses the adaptive arm of the immune system, i.e. T cells that
are necessary to kill virus-infected cells. This creates a vicious cycle that
prevents a specific immune response against SARS-CoV-2. The key role of oxidative
stress in the pathogenesis of severe COVID-19 implies that therapeutic
counterbalancing of ROS by antioxidants such as vitamin C or NAC and/or by
antagonizing ROS production by cells of the mononuclear phagocyte system (MPS)
and neutrophil granulocytes and/or by blocking of TNF-? can prevent COVID-19 from
becoming severe. Controlled clinical trials and preclinical models of COVID-19
are needed to evaluate this hypothesis.
free
free
free
