NLRP3 inflammasome activation in COVID-19: an interlink between risk factors and disease severity

Amin, Saiful; Aktar, Salma; Rahman, Md. Mijanur; Chowdhury, Mohammed

doi:10.1016/j.micinf.2021.104913

Cited by 33 publications

(28 citation statements)

References 98 publications

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“…NLRP3 is the central protein platform for caspase-1 activation, leading to the proteolytic maturation of IL-1β and IL-18. The inflammasome induces an inflammatory cell death termed pyroptosis [ 12 , 36 , 40 , 41 ] ( Figure 1 C). IL-18 also acts as neutrophil-attracting to favor its continuous infiltration in infected lungs; thus, neutrophils are activated by IL-17, and they can form neutrophil extracellular trap (NET), a cell death type precisely in neutrophils, and it is called NETosis, where several intracellular components are released as neutrophil elastase, cathepsins, lactoferrin, myeloperoxidase, and granule proteins.…”

Section: More Than One Rout Favor the Cytokine Storm In Covid-19mentioning

confidence: 99%

Immunosuppressant Therapies in COVID-19: Is the TNF Axis an Alternative?

Palacios

Chávez‐Galán

2022

Pharmaceuticals

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The study of cytokine storm in COVID-19 has been having different edges in accordance with the knowledge of the disease. Various cytokines have been the focus, especially to define specific treatments; however, there are no conclusive results that fully support any of the options proposed for emergency treatment. One of the cytokines that requires a more exhaustive review is the tumor necrosis factor (TNF) and its receptors (TNFRs) as increased values of soluble formats for both TNFR1 and TNFR2 have been identified. TNF is a versatile cytokine with different impacts at the cellular level depending on the action form (transmembrane or soluble) and the receptor to which it is associated. In that sense, the triggered mechanisms can be diversified. Furthermore, there is the possibility of the joint action provided by synergism between one or more cytokines with TNF, where the detonation of combined cellular processes has been suggested. This review aims to discuss some roles of TNF and its receptors in the pro-inflammatory stage of COVID-19, understand its ways of action, and let to reposition this cytokine or some of its receptors as therapeutic targets.

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Section: More Than One Rout Favor the Cytokine Storm In Covid-19mentioning

confidence: 99%

Immunosuppressant Therapies in COVID-19: Is the TNF Axis an Alternative?

Palacios

Chávez‐Galán

2022

Pharmaceuticals

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“…Recent articles have also highlighted the potential role of NLRP3-inflammasome in COVID-19. For example, studies have investigated the role of non-coding RNAs in the regulation of NLRP3-inflammasome complex in COVID-19, the relationship between NL-RP3-inflammasome and probiotics in COVID-19, the various aspects of inflammasomes as role players in COVID-19, and the potential role of the NLRP3-inflammasomes in COVID-19 [32][33][34][35][36][37][38][39][40][41]. Interestingly, a recent study has shown that specific suppression of the NLRP3-inflammasome represses the immune over-activation and diminishes COVID-19-like pathology in mice [42].…”

Section: Hyperactivity Of Nlrp3-inflammasome; a Key Factor In Covid-1...mentioning

confidence: 99%

COVID-19-induced immune thrombocytopenic purpura; Immunopathogenesis and clinical implications

et al. 2022

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Following the outbreak of the COVID-19 pandemic, millions of people around the world have been affected with SARS-CoV-2 infection. In addition to the typical symptoms, thrombotic events, lymphopenia, and thrombocytopenia have been reported in COVID-19 patients. Immune thrombocytopenic purpura (ITP) is one of the thrombotic events that occur in some COV-ID-19 patients. Hyperinflammation, cytokine storms, and immune dysregulation in some patients are the cause to the main COVID-19 complications such as ALI (acute lung injury), acute respiratory distress syndrome (ARDS), and multiple organ failure. Disruption in the differentiation of T-cells, enhanced differentiation of Th17 and Th1, cell death (pyroptosis), SUMMARYhyper-inflammation and dysfunction of inflammatory neutrophils and macrophages, and hyperactivity of NLRP3-inflammasome are among the important factors that may be the cause to COVID-19-induced ITP. This study aimed to give an overview of the findings on the immunopathogenesis of ITP and COVID-19-induced ITP. Further studies are required to better understand the exact immunopathogenesis and effective treatments for ITP, especially in inflammatory disorders.

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“…Thus, it can be used as a potential therapeutic target in COVID-19, particularly in combination with antivirals ( 6 , 7 ). Recently published articles conducted on various aspects of the role of Inflammasomes in covid19 and the potential role of the NLRP3 Inflammasomes ( 8 , 9 , 10 ). A recent study has interestingly shown Specific suppression of the NLRP3 inflammasome repress immune overactivation and diminish COVID-19 like pathology in mice ( 11 ).…”

Section: Introductionmentioning

confidence: 99%