Neutrophils and Neutrophil Extracellular Traps Drive Necroinflammation in COVID-19

Tomar, Bhawna; Anders, Hans‐Joachim; Desai, Jyaysi; Mulay, Shrikant R.

doi:10.3390/cells9061383

Cited by 245 publications

(240 citation statements)

References 53 publications

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“…Although our understanding of the host immune responses to the novel SARS-CoV-2 virus is increasing by leaps, thanks to the momentum gained by global research efforts, it is still limited, particularly in the field of innate immune mechanisms. Earlier studies demonstrated major neutrophilia and enhanced levels of neutrophil-associated chemokines (IL-8, CXCL2, or G-CSF) [ 3 , 30 ], and pointed towards the involvement of neutrophils via the mechanisms of NETosis and necroptosis [ 8 , 12 , 31 , 32 ]. The most recent data from transcriptomic analyses also suggest that monocytes, T, NK, and dendritic cells are likely not the principal drivers of cytokine-mediated hyperinflammation [ 9 , 13 , 33 ] and therefore, neutrophils gradually profile as the major culprits.…”

Section: Discussionmentioning

confidence: 99%

Disharmonic Inflammatory Signatures in COVID-19: Augmented Neutrophils’ but Impaired Monocytes’ and Dendritic Cells’ Responsiveness

Paračková

Zentsová

Bloomfield

et al. 2020

Cells

122

145

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COVID-19, caused by SARS-CoV-2 virus, emerged as a pandemic disease posing a severe threat to global health. To date, sporadic studies have demonstrated that innate immune mechanisms, specifically neutrophilia, NETosis, and neutrophil-associated cytokine responses, are involved in COVID-19 pathogenesis; however, our understanding of the exact nature of this aspect of host–pathogen interaction is limited. Here, we present a detailed dissection of the features and functional profiles of neutrophils, dendritic cells, and monocytes in COVID-19. We portray the crucial role of neutrophils as drivers of hyperinflammation associated with COVID-19 disease via the shift towards their immature forms, enhanced degranulation, cytokine production, and augmented interferon responses. We demonstrate the impaired functionality of COVID-19 dendritic cells and monocytes, particularly their low expression of maturation markers, increased PD-L1 levels, and their inability to upregulate phenotype upon stimulation. In summary, our work highlights important data that prompt further research, as therapeutic targeting of neutrophils and their associated products may hold the potential to reduce the severity of COVID-19.

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Section: Discussionmentioning

confidence: 99%

Disharmonic Inflammatory Signatures in COVID-19: Augmented Neutrophils’ but Impaired Monocytes’ and Dendritic Cells’ Responsiveness

Paračková

Zentsová

Bloomfield

et al. 2020

Cells

122

145

View full text Add to dashboard Cite

show abstract

“…Furthermore, this ratio could be used as a marker for predicting whether more severe complications such as ARDS would arise ( Lagunas-Rangel, 2020 ). Finally, neutrophils are suggested as a target for immunopathologic complications in severe COVID-19 patients ( Tomar et al, 2020 ). The elevated neutrophil count in COVID-19 patients and its significant correlation with disease severity indicates the importance of neutrophils in the management of COVID-19.…”

Section: Contribution Of Neutrophils To Covid-19 Associated Ardsmentioning

confidence: 99%

Targeting Neutrophils to Treat Acute Respiratory Distress Syndrome in Coronavirus Disease

et al. 2020

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This review describes targeting neutrophils as a potential therapeutic strategy for acute respiratory distress syndrome (ARDS) associated with coronavirus disease 2019 (COVID-19), a pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Neutrophil counts are significantly elevated in patients with COVID-19 and significantly correlated with disease severity. The neutrophil-to-lymphocyte ratio can serve as a clinical marker for predicting fatal complications related to ARDS in patients with COVID-19. Neutrophil-associated inflammation plays a critical pathogenic role in ARDS. The effector functions of neutrophils, acting as respiratory burst oxidants, granule proteases, and neutrophil extracellular traps, are linked to the pathogenesis of ARDS. Hence, neutrophils can not only be used as pathogenic markers but also as candidate drug targets for COVID-19 associated ARDS.

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“…milieu (Barnes et al, 2020;Mozzini & Girelli, 2020;Thierry, 2020;Thierry & Roch, 2020;Tomar, Anders, Desai, & Mulay, 2020). Indeed, there is a high degree of NET-IL-1β interplay during both venous and arterial thrombosis and severe asthma (Lachowicz-Scroggins et al, 2019;Liberale et al, 2019;Yadav et al, 2019), and it has been hypothesised that there may be therapeutic potential in targeting the IL-1β/NET feedback loop (Yaqinuddin & Kashir, 2020).…”

Section: Pge 2 On Net Releasementioning

confidence: 99%

Non‐steroidal anti‐inflammatory drugs, prostaglandins, and COVID‐19

Robb

Goepp

Rossi

et al. 2020

British J Pharmacology

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the novel coronavirus disease 2019 (COVID-19), a highly pathogenic and sometimes fatal respiratory disease responsible for the current 2020 global pandemic. Presently, there remains no effective vaccine or efficient treatment strategies against COVID-19. Non-steroidal anti-inflammatory drugs (NSAIDs) are medicines very widely used to alleviate fever, pain, and inflammation (common symptoms of COVID-19 patients) through effectively blocking production of prostaglandins (PGs) via inhibition of cyclooxyganase enzymes. PGs can exert either proinflammatory or anti-inflammatory effects depending on the inflammatory scenario. In this review, we survey the potential roles that NSAIDs and PGs may play during SARS-CoV-2 infection and the development and progression of COVID-19.

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Neutrophils and Neutrophil Extracellular Traps Drive Necroinflammation in COVID-19

Cited by 245 publications

References 53 publications

Disharmonic Inflammatory Signatures in COVID-19: Augmented Neutrophils’ but Impaired Monocytes’ and Dendritic Cells’ Responsiveness

Disharmonic Inflammatory Signatures in COVID-19: Augmented Neutrophils’ but Impaired Monocytes’ and Dendritic Cells’ Responsiveness

Targeting Neutrophils to Treat Acute Respiratory Distress Syndrome in Coronavirus Disease

Non‐steroidal anti‐inflammatory drugs, prostaglandins, and COVID‐19

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