What about COVID-19 and arachidonic acid pathway?

Hoxha, Malvina

doi:10.1007/s00228-020-02941-w

Cited by 70 publications

(78 citation statements)

References 28 publications

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“…Cyclooxygenase-2 (COX-2) is a rate-limiting enzyme for the generation of PGE2 and Hydroxyprostaglandin Dehydrogenase 15-(NAD) (HPGD) is an enzyme responsible for the degradation of PGE2 29 . These ndings, supported further by a recent literature review 30 naturally suggested a connection between arachidonic acid metabolism and PGE2 in COVID-19 disease.…”

Section: Introductionsupporting

confidence: 69%

SARS-CoV-2-induced impaired immune response by Prostaglandin E2 is accelerated by age, male sex and air pollution

Ricke‐Hoch

Stelling

Laßwitz

et al. 2020

Preprint

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The SARS-CoV-2 coronavirus has led to a pandemic with millions of people affected. The present study finds prostaglandin E2 (PGE2) blood levels elevated in COVID-19 patients with positive correlation with disease severity. SARS-CoV-2 induces PGE2 generation and secretion in infected lung epithelial cells by upregulating cyclo-oxygenase (COX)-2 and reducing the PG-degrading enzyme 15-hydroxyprostaglandin-dehydrogenase. Also living human-lung-precision-slices infected with SARS-CoV-2 display upregulated COX-2. PGE2 in serum of COVID-19 patients lowers the expression of Paired-Box-Protein-Pax-5 (PAX5), a master regulator of B-cell survival, proliferation and differentiation, in both human and mouse pre-B-cells, while the PGE2 inhibitor taxifolin directly reduces SARS-CoV-2-induced PGE2 production and attenuates viral replication. Risk-factors for severe disease courses, i.e. older age, male sex and air pollution are associated with higher PGE2 production and lower PAX5 expression in pre-B-cells. Since PGE2 acts broadly immunosuppressive its elevation might reduce the early anti-viral defense and its inhibition may therefore reduce severe disease courses.

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Section: Introductionsupporting

confidence: 69%

SARS-CoV-2-induced impaired immune response by Prostaglandin E2 is accelerated by age, male sex and air pollution

Ricke‐Hoch

Stelling

Laßwitz

et al. 2020

Preprint

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“…Beyond the proinflammatory cytokines, also the products of lipid metabolism, namely arachidonic acid (AA) derivates—prostaglandins, leukotrienes, and thromboxane—act as proinflammatory mediators in COVID-19 and AA-deficient patients are more susceptible to a severe course of SARS-CoV-2 infection [ 59 ]. However, more studies are needed to elucidate the involvement of these pathways since inhibiting AA mediators brought conflicting results and other studies have questioned the role of AA inhibitors, such as nonsteroidal anti-inflammatory drugs (NSAID) and ibuprofen, in the worsening of COVID-19 [ 60 ].…”

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

125

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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“…The hijacking of the cellular amino acid metabolism to fuel viral proliferation might be a critical mechanism underlying the COVID-19 pathogenesis [ 34 ]. Arachidonic acid is an endogenous bioactive antiviral lipid, and this metabolic pathway has been suggested to play an important role in susceptibility to COVID-19 [ 35 , 36 ]. The elevated levels of free poly-unsaturated fatty acids are characteristics of COVID-19 patients [ 10 , 37 ].…”

Section: Discussionmentioning

confidence: 99%

Comprehensive Meta-Analysis of COVID-19 Global Metabolomics Datasets

et al. 2021

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The novel coronavirus SARS-CoV-2 has spread across the world since 2019, causing a global pandemic. The pathogenesis of the viral infection and the associated clinical presentations depend primarily on host factors such as age and immunity, rather than the viral load or its genetic variations. A growing number of omics studies have been conducted to characterize the host immune and metabolic responses underlying the disease progression. Meta-analyses of these datasets have great potential to identify robust molecular signatures to inform clinical care and to facilitate therapeutics development. In this study, we performed a comprehensive meta-analysis of publicly available global metabolomics datasets obtained from three countries (United States, China and Brazil). To overcome high heterogeneity inherent in these datasets, we have (a) implemented a computational pipeline to perform consistent raw spectra processing; (b) conducted meta-analyses at pathway levels instead of individual feature levels; and (c) performed visual data mining on consistent patterns of change between disease severities for individual studies. Our analyses have yielded several key metabolic signatures characterizing disease progression and clinical outcomes. Their biological interpretations were discussed within the context of the current literature. To the best of our knowledge, this is the first comprehensive meta-analysis of global metabolomics datasets of COVID-19.

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What about COVID-19 and arachidonic acid pathway?

Cited by 70 publications

References 28 publications

SARS-CoV-2-induced impaired immune response by Prostaglandin E2 is accelerated by age, male sex and air pollution

SARS-CoV-2-induced impaired immune response by Prostaglandin E2 is accelerated by age, male sex and air pollution

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

Comprehensive Meta-Analysis of COVID-19 Global Metabolomics Datasets

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