COVID-19 stokes inflammasomes

Bryant, Clare

doi:10.1084/jem.20202413

Cited by 7 publications

(9 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, COVID-19 stokes inflammasomes and [83] the relevance of NLRP3 inflammasomes as a potential therapeutic target to manage clinical manifestation of COVID-19 have been discussed [84].…”

Section: Inflammasomesmentioning

confidence: 99%

How Do Inflammatory Mediators, Immune Response and Air Pollution Contribute to COVID-19 Disease Severity? A Lesson to Learn

Signorini

Pignatti

Coccini

2021

Life

View full text Add to dashboard Cite

Inflammatory and immune processes are defensive mechanisms that aim to remove harmful agents. As a response to infections, inflammation and immune response contribute to the pathophysiological mechanisms of diseases. Coronavirus disease 2019 (COVID-19), whose underlying mechanisms remain not fully elucidated, has posed new challenges for the knowledge of pathophysiology. Chiefly, the inflammatory process and immune response appear to be unique features of COVID-19 that result in developing a hyper-inflammatory syndrome, and air pollution, the world’s largest health risk factor, may partly explain the behaviour and fate of COVID-19. Understanding the mechanisms involved in the progression of COVID-19 is of fundamental importance in order to avoid the late stage of the disease, associated with a poor prognosis. Here, the role of the inflammatory and immune mediators in COVID-19 pathophysiology is discussed.

show abstract

“…Thus, COVID-19 stokes inflammasomes and [83] the relevance of NLRP3 inflammasomes as a potential therapeutic target to manage clinical manifestation of COVID-19 have been discussed [84].…”

Section: Inflammasomesmentioning

confidence: 99%

How Do Inflammatory Mediators, Immune Response and Air Pollution Contribute to COVID-19 Disease Severity? A Lesson to Learn

Signorini

Pignatti

Coccini

2021

Life

View full text Add to dashboard Cite

show abstract

“…2). 41,43 The activation of NLRP3 inflammasome and LDH release indicates potential activation of the pyroptosis along with other lytic cell death programs during SARS-CoV-2 infection and in COVID-19. Additional studies monitoring the activation of GSDMD and testing SARS-CoV2 infection in Gsdmd -/cells deliver the specific contribution of pyroptosis and other cell death mechanisms in mediating the release of LDH and other DAMPs.…”

Section: The Inflammasome Activation and Covid-19 Severitymentioning

confidence: 99%

“…The prominent activation of the NLRP3 inflammasome is observed in response to the SARS-CoV-2 infection and is active in COVID-19 patients who require hospitalization. 41,43 Higher levels of CASP1, IL-1β, and IL-18 are seen in COVID-19 patients compared with healthy individuals. 12,15,41,45 Analyzing peripheral blood mononuclear cells isolated from COVID-19 patients indicates the active inflammasome and CASP1 in lethal cases of COVID-19.…”

Section: The Inflammasome Activation and Covid-19 Severitymentioning

confidence: 99%

“…It remains to be established whether pathogenic human CoVs, like SARS‐CoV‐2, engage PANoptosis. The prominent activation of the NLRP3 inflammasome is observed in response to the SARS‐CoV‐2 infection and is active in COVID‐19 patients who require hospitalization 41,43 . Higher levels of CASP1, IL‐1β, and IL‐18 are seen in COVID‐19 patients compared with healthy individuals 12,15,41,45 .…”

Section: The Inflammasome Activation and Covid‐19 Severitymentioning

confidence: 99%

See 1 more Smart Citation

Inflammasome regulation in driving COVID-19 severity in humans and immune tolerance in bats

Nagaraja

Jain

Kesavardhana

2021

Journal of Leukocyte Biology

View full text Add to dashboard Cite

Coronaviruses (CoVs) are RNA viruses that cause human respiratory infections. Zoonotic transmission of the SARS‐CoV‐2 virus caused the recent COVID‐19 pandemic, which led to over 2 million deaths worldwide. Elevated inflammatory responses and cytotoxicity in the lungs are associated with COVID‐19 severity in SARS‐CoV‐2‐infected individuals. Bats, which host pathogenic CoVs, operate dampened inflammatory responses and show tolerance to these viruses with mild clinical symptoms. Delineating the mechanisms governing these host‐specific inflammatory responses is essential to understand host–virus interactions determining the outcome of pathogenic CoV infections. Here, we describe the essential role of inflammasome activation in determining COVID‐19 severity in humans and innate immune tolerance in bats that host several pathogenic CoVs. We further discuss mechanisms leading to inflammasome activation in human SARS‐CoV‐2 infection and how bats are molecularly adapted to suppress these inflammasome responses. We also report an analysis of functionally important residues of inflammasome components that provide new clues of bat strategies to suppress inflammasome signaling and innate immune responses. As spillover of bat viruses may cause the emergence of new human disease outbreaks, the inflammasome regulation in bats and humans likely provides specific strategies to combat the pathogenic CoV infections.

show abstract

“…There is some evidence that SARS-CoV-2 stimulates the inflammasomes, a group of multimeric protein complexes which are responsive to pathogen-associated molecular patters (PAMPs), damage-associated molecular patterns (DAMPs) and environmental toxins [2, 7]. In COVID-19, the NLRP3 inflammasome is activated in response to SARS-CoV-2 infection as discovered in postmortem PBMCs and tissues of patients with moderate and critical COVID-19 [7,8,9]. NLRP3 or NOD, LRR (leucine rich repeat domain) and pyrin domain-containing protein 3 is an intracellular sensor which is primed by cellular stress via PAMPs (bacterial, viral and fungal infections) and DAMPs, resulting in the formation of the NLRP3 inflammasome with elevated levels of caspase-1, IL-1, and IL-18 and increased pyroptosis, an inflammatory form of cell death [9, 10].…”

Section: Introductionmentioning

confidence: 99%

In COVID-19, NLRP3 inflammasome genetic variants are associated with critical disease and these effects are partly mediated by the sickness symptom complex: a nomothetic network approach

Maes

Tedesco

Lozovoy

et al. 2021

Preprint

View full text Add to dashboard Cite

Background: In COVID-19, the NLRP3 inflammasome is activated in response to SARS-CoV-2 infection. Acute infections are accompanied by a sickness symptom complex (SSC) which is a highly conserved symptom complex that protects against infections and hyperinflammation. Aims: To examine the associations of COVID-19, SSC and the NLPR3 rs10157379 T>C and NLPR3 rs10754558 C>G SNV variants; and the protective role of SSC in severe acute respiratory syndrome (SARS)-CoV-2 infection. Methods: We recruited COVID-19 patients, 308 with critical, 63 with moderate and 157 with mild disease. Results: Increased SSC protects against SARS, critical disease, and death due to COVID-19. Increasing age, male sex and rs10754558 CG significantly predict reduced SSC protection. The rs10157379 CT and rs10754558 GG genotypes are positively associated with SARS. Partial Least Squares analysis shows a) that 41.8% of the variance in critical COVID-19 symptoms could be explained by SSC and oxygen saturation (inversely associated), and inflammation, chest computed tomography abnormalities, increased body mass index, SARS and age (positively associated); and b) the effects of the NLRP3 rs10157379 and rs10754558 variants on critical COVID-19 are mediated via SSC (protective) and SARS (detrimental). SSC includes anosmia, dysgeusia and gastrointestinal symptoms. Conclusions: Intersections among the rs10754558 variant, age, and sex increase risk towards critical COVID-19 by attenuating SSC. NLRP3 variants play an important role in SARS, and severe and critical COVID-19 especially in individuals with reduced SSC, elderly people, and those with increased BMI, hypertension, and diabetes type 2. SSC is a new drug target to combat acute COVID-19.

show abstract

COVID-19 stokes inflammasomes

Cited by 7 publications

References 16 publications

How Do Inflammatory Mediators, Immune Response and Air Pollution Contribute to COVID-19 Disease Severity? A Lesson to Learn

How Do Inflammatory Mediators, Immune Response and Air Pollution Contribute to COVID-19 Disease Severity? A Lesson to Learn

Inflammasome regulation in driving COVID-19 severity in humans and immune tolerance in bats

In COVID-19, NLRP3 inflammasome genetic variants are associated with critical disease and these effects are partly mediated by the sickness symptom complex: a nomothetic network approach

Contact Info

Product

Resources

About