How NETosis could drive “Post-COVID-19 syndrome” among survivors

Sawadogo, Serge A; Dighero-Kemp, Bonnie; Ouédraogo, Dieu-Donné; Hensley, Lisa E.; Sakandé, Jean

doi:10.1016/j.imlet.2020.09.005

Cited by 34 publications

(22 citation statements)

References 31 publications

(40 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, a delayed-phase thrombocytopenia of putative immune origin has been reported in 11.8% among 271 patients with COVID-19 [118]. Aberrant release of neutrophil extracellular traps (NETs) consisting of myeloperoxidase-and neutrophil elastase-containing granules could be seen in COVID-19 [119]. The non-specific action of NETs along with the concomitant release of auto-antigens by apoptotic neutrophils could also stimulate auto-immunity and normal tissue damage [119].…”

Section: Inflammatory Autoimmune and Rheumatological Complicationsmentioning

confidence: 99%

Epidemiology and organ specific sequelae of post-acute COVID19: A narrative review

Korompoki

Gavriatopoulou

Hicklen

et al. 2021

Journal of Infection

127

View full text Add to dashboard Cite

This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

show abstract

Section: Inflammatory Autoimmune and Rheumatological Complicationsmentioning

confidence: 99%

Epidemiology and organ specific sequelae of post-acute COVID19: A narrative review

Korompoki

Gavriatopoulou

Hicklen

et al. 2021

Journal of Infection

127

View full text Add to dashboard Cite

show abstract

“…The authors suggest that low-grade inflammation associated with endothelial activation status may persist following SARS-CoV-2 infection, posing a risk of thrombotic events [62,63]. Sawadogo et al (2020) points out that if research confirms NETs as the leading cause of the severe and fatal course of COVID-19, perhaps we should prepare to define a new non-communicable inflammatory disease among convalescents-"Post-COVID-19 Syndrome". The authors suggest the need to monitor NETs biomarkers, but also to extend the research to the evaluation of autoimmune markers: ANCA, anti-cyclic citrullinated peptide, rheumatoid factor, and anti-NET antibodies (ANETA) [64].…”

Section: Nets and Covid-19 Progression In People With Concurrent Diseasesmentioning

confidence: 99%

Significance of NETs Formation in COVID-19

Janiuk

Jabłońska

Garley

2021

Cells

View full text Add to dashboard Cite

Severe contagious respiratory disease—COVID-19—caused by the SARS-CoV-2 coronavirus, can lead to fatal respiratory failure associated with an excessive inflammatory response. Infiltration and spread of SARS-CoV-2 are based on the interaction between the virus’ structural protein S and the cell’s receptor–angiotensin-converting enzyme 2 (ACE2), with the simultaneous involvement of human trans-membrane protease, serine 2 (TMPRSS2). Many scientific reports stress the importance of elevated recruitment and activity of neutrophils, which can form extracellular neutrophil traps (NETs) playing a significant role in the mechanism of combating pathogens, in the pathogenesis of COVID-19. Excessive generation of NETs during prolonged periods of inflammation predisposes for the occurrence of undesirable reactions including thromboembolic complications and damage to surrounding tissues and organs. Within the present manuscript, we draw attention to the impact of NET generation on the severe course of COVID-19 in patients with concurrent cardiovascular and metabolic diseases. Additionally, we indicate the necessity to explore not only the cellular but also the molecular bases of COVID-19 pathogenesis, which may aid the development of dedicated therapies meant to improve chances for the successful treatment of patients. We also present new directions of research into medications that display NETs formation regulatory properties as potential significant therapeutic strategies in the progress of COVID-19.

show abstract

“…It has been shown that innate activation by viral infections can cause flares of diseases with predominant autoinflammatory pathogenesis like psoriasis [ 42 ]. NETosis has been proposed in the causation of post-COVID-19 syndrome [ 43 ]. Also, there is some evidence that the SARS-CoV-2 infection is aided by autoantibodies such as anti-interferon antibodies that are found in about 10% of severe COVID-19 cases [ 44 ].…”

Section: Introductionmentioning

confidence: 99%

COVID-19 and the clinical course of rheumatic manifestations

2021

View full text Add to dashboard Cite

The manifestations of COVID-19 have been evolving over time. Various post-COVID-19 syndromes are being recognised. Various viruses have been implicated in the pathogenesis of autoimmune diseases, and we expect a similar outcome with the severe acute respiratory syndrome-associated coronavirus-2 (SARS-CoV-2). The SARS-CoV-2 virus penetrates various tissues and organs and has a predisposition to lead to endotheliitis that may cause vascular manifestations including thrombosis. SARS-CoV-2 has been shown to activate Toll-like receptors and the complement system. It perpetuates NETosis and leads to autoantibody formation. These predispose to systemic autoimmunity. Both reactive arthritis and connective tissue disorders such as lupus and inflammatory myositis have been reported after COVID-19. Other reported autoimmune disorders include haemolytic anaemia, immune thrombocytopenia, cutaneous vasculitis, and Guillain Barré-like acute demyelinating disorders. The multisystem inflammatory syndrome in children and its adult counterpart are another post-COVID-19 entity that presents as an admixture of Kawasaki disease and staphylococcal toxic shock syndrome. Patients with preexisting rheumatic diseases may flare during the SARS-CoV-2 infection. They may develop novel autoimmune features also. The immune-suppressants used during the acute COVID-19 illness may confound the outcomes whereas comorbidities present in patients with rheumatic diseases may mask them. There is an urgent need to follow-up patients recovering from COVID and monitor autoantibody production in the context of rheumatic manifestations. Key Points • COVID-19 is associated with both innate and acquired immune reactions and production of various autoantibodies. • Various immune-mediated manifestations such as arthritis, myositis, haemolytic anaemia, thrombocytopenia, and acute demyelination may develop after COVID-19. • Longitudinal cohort data are warranted to describe, predict, and test prevent various rheumatic manifestations in post-COVID-19 subjects.

show abstract

How NETosis could drive “Post-COVID-19 syndrome” among survivors

Cited by 34 publications

References 31 publications

Epidemiology and organ specific sequelae of post-acute COVID19: A narrative review

Epidemiology and organ specific sequelae of post-acute COVID19: A narrative review

Significance of NETs Formation in COVID-19

COVID-19 and the clinical course of rheumatic manifestations

Contact Info

Product

Resources

About