Dexamethasone alleviate allergic airway inflammation in mice by inhibiting the activation of NLRP3 inflammasome

Guan, Minglong; Ma, Hengli; Fan, Xiaoning; Chen, Xu; Miao, Manli; Wu, Hui-Mei

doi:10.1016/j.intimp.2019.106017

Cited by 45 publications

(33 citation statements)

References 39 publications

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“…Up to now, six clinical trials (NCT04347980, NCT04325061, NCT04395105, NCT04344730, NCT04360876, and NCT04327401) reported on clinicaltrials.gov are recruiting patients to test the efficacy of the corticosteroid dexamethasone, whose beneficial effects in airway inflammation have been recently demonstrated to involve lung inhibition of the activity of NLRP3 inflammasome and the release of IL‐1β and IL‐18 (M. Guan, Ma, et al, 2020).…”

Section: The Nlrp3 Inflammasome and Pharmacological Treatments For Comentioning

confidence: 99%

The hidden role of NLRP3 inflammasome in obesity‐related COVID‐19 exacerbations: Lessons for drug repurposing

Bertocchi

Foglietta

Collotta

et al. 2020

British J Pharmacology

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COVID-19, the illness caused by SARS-CoV-2, has a wide-ranging clinical spectrum that, in the worst-case scenario, involves a rapid progression to severe acute respiratory syndrome and death. Epidemiological data show that obesity and diabetes are among the main risk factors associated with high morbidity and mortality. The increased susceptibility to SARS-CoV-2 infection documented in obesity-related metabolic derangements argues for initial defects in defence mechanisms, most likely due to an elevated systemic metabolic inflammation ("metaflammation"). The NLRP3 inflammasome is a master regulator of metaflammation and has a pivotal role in the pathophysiology of either obesity or diabetes. Here, we discuss the most recent findings suggesting contribution of NLRP3 inflammasome to the increase in complications in COVID-19 patients with diabesity. We also review current pharmacological strategies for COVID-19, focusing on treatments whose efficacy could be due, at least in part, to interference with the activation of the NLRP3 inflammasome.

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Section: The Nlrp3 Inflammasome and Pharmacological Treatments For Comentioning

confidence: 99%

The hidden role of NLRP3 inflammasome in obesity‐related COVID‐19 exacerbations: Lessons for drug repurposing

Bertocchi

Foglietta

Collotta

et al. 2020

British J Pharmacology

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show abstract

“…On the other hand, there are some therapies that are already FDA-approved and have been shown to interfere with inflammasome signaling activation which are already being considered for the treatment of COVID-19 such as Enoxaparin ( 161 , 162 ), anakinra ( 168 ), tocilizumab ( 168 ), and dexamethasone ( 159 , 160 ). Moreover, another drug that is already approved by the FDA that can also be used to inhibit the inflammasome is IFN-β ( 163 ), which is already used to treat multiple sclerosis ( 169 ), and is currently being tested for its effects on COVID-19 patients ( 164 ).…”

Section: Discussionmentioning

confidence: 99%

The Inflammasome in Times of COVID-19

Vaccari¹,

et al. 2020

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Coronaviruses (CoVs) are members of the genus Betacoronavirus and the Coronaviridiae family responsible for infections such as severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and more recently, coronavirus disease-2019 (COVID-19). CoV infections present mainly as respiratory infections that lead to acute respiratory distress syndrome (ARDS). However, CoVs, such as COVID-19, also present as a hyperactivation of the inflammatory response that results in increased production of inflammatory cytokines such as interleukin (IL)-1β and its downstream molecule IL-6. The inflammasome is a multiprotein complex involved in the activation of caspase-1 that leads to the activation of IL-1β in a variety of diseases and infections such as CoV infection and in different tissues such as lungs, brain, intestines and kidneys, all of which have been shown to be affected in COVID-19 patients. Here we review the literature regarding the mechanism of inflammasome activation by CoV infection, the role of the inflammasome in ARDS, ventilator-induced lung injury (VILI), and Disseminated Intravascular Coagulation (DIC) as well as the potential mechanism by which the inflammasome may contribute to the damaging effects of inflammation in the cardiac, renal, digestive, and nervous systems in COVID-19 patients.

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“…Lung damage scoring criteria: 0 point, normal tissue; 1 point, focal interstitial hyperemia and inflammatory cells infiltration; 2 points, diffuse interstitial hyperemia and inflammatory cells infiltration; 3 points, alveolar wall capillary dilatation and hyperemia, alveolar wall widening (inflammatory cell infiltration/fibrosis); 4 points, alveolar wall capillary dilation and hyperemia, alveolar wall widening (inflammatory cell infiltration/fibrosis), alveolar cavity exudation, alveolar consolidation, accompanied by infiltration of inflammatory exudates in bronchial cavity (14). Lung inflammation scoring criteria: 0 point, normal tissue; 1 point, a few cells; 2 points, a ring of inflammatory cells 1 cell layer deep; 3 points, a ring of inflammatory cells 2-4 cells deep, and 4 points, a ring of inflammatory cells >4 cells deep (15).…”

Section: Histological Analysismentioning

confidence: 99%

TRIM59 Protects Mice From Sepsis by Regulating Inflammation and Phagocytosis in Macrophages

et al. 2020

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Sepsis is associated with bacterial invasion and inflammation and has a high mortality rate. Previous studies have demonstrated that tripartite motif 59 (TRIM59) was involved in NF-κB signaling and could promote phagocytosis of macrophages, but the role of TRIM59 in sepsis is still unknown. In our study, we found that TRIM59 was downregulated in lipopolysaccharide (LPS)-stimulated bone marrow-derived macrophages (BMDMs). In the cecal ligation and puncture (CLP) sepsis mice model, the mortality of Trim59 flox/flox Lyz-Cre (Trim59-cKO) mice was higher, the immune cell infiltration and damage of liver and lung were more severe, and bacteria burden was increased. We also found that TRIM59 altered the production of pro-inflammation cytokines, as well as macrophage phagocytosis ability. Further analysis indicated that NF-κB signal pathway and Fcγ receptors might be involved in these regulations. Our study demonstrated for the first time that TRIM59 protects mice from sepsis by regulating inflammation and phagocytosis in macrophages.

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Dexamethasone alleviate allergic airway inflammation in mice by inhibiting the activation of NLRP3 inflammasome

Cited by 45 publications

References 39 publications

The hidden role of NLRP3 inflammasome in obesity‐related COVID‐19 exacerbations: Lessons for drug repurposing

The hidden role of NLRP3 inflammasome in obesity‐related COVID‐19 exacerbations: Lessons for drug repurposing

The Inflammasome in Times of COVID-19

TRIM59 Protects Mice From Sepsis by Regulating Inflammation and Phagocytosis in Macrophages

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