- |||||||||| Bay11-7082 / InvivoGen
Preclinical, Journal: Inhibition of NLRP3 inflammasome attenuates spinal cord injury-induced lung injury in mice. (Pubmed Central) - Mar 31, 2020 In brief, our results showed that, NLRP3 inflammasome inhibitor BAY 11-7082 or A438079 inhibited activation of NLRP3 inflammasome, alleviated mitochondrial dysfunction, the number of macrophage and neutrophil, thereby attenuating alveolar type II cell apoptosis, lung edema, and histological injury. Taken together, our data reveal that NLRP3 inflammasome inhibitor BAY 11-7082 or A438079 attenuates the inflammatory response, reverses mitochondrial dysfunction, and subsequently alleviates secondary lung injury following SCI.
- |||||||||| Clinical, Journal: Increased neutrophil extracellular traps activate NLRP3 and inflammatory macrophages in adult-onset Still's disease. (Pubmed Central) - Mar 31, 2020
Taken together, our data reveal that NLRP3 inflammasome inhibitor BAY 11-7082 or A438079 attenuates the inflammatory response, reverses mitochondrial dysfunction, and subsequently alleviates secondary lung injury following SCI. These findings implicate accelerated NET formation in AOSD pathogenesis through activation of NLRP3 and proinflammatory macrophages, and identify a novel link between neutrophils and macrophages by NET formation in AOSD.
- |||||||||| Kineret (anakinra) / SOBI, Affibody, digoxin / Generic mfg.
Journal: Inflammasome inhibition blocks cardiac glycoside cell toxicity. (Pubmed Central) - Mar 31, 2020 Our results inform on the molecular mechanism by which the inflammasome integrates the diverse signals that activate it through secondary signals like cation flux. Furthermore, this mechanism suggests a contribution of the inflammasome to the toxicity and adverse events associated with cardiac glycosides use in humans, and that targeted anti-inflammatories could provide an additional adjunct therapeutic countermeasure.
- |||||||||| Tamoxis (tamoxifen) / Bioprofarma
Journal: Tamoxifen-induced, intestinal-specific deletion of Slc5a6 in adult mice leads to spontaneous inflammation: Involvement of NF-kB, NLRP3, and gut microbiota. (Pubmed Central) - Mar 31, 2020 Notably, administration of broad-spectrum antibiotics reduced lethality and led to normalization of intestinal inflammation, pro-inflammatory cytokines, altered mucosal integrity, and reduced expression of the NLRP3 inflammasome. Overall, these findings support our conclusion that the biotin transport pathway plays an important role in the maintenance of intestinal homeostasis, and that NF-κB, the NLRP3 inflammasome, as well as gut microbiota drive the development of intestinal inflammation when SMVT is absent.
- |||||||||| allopurinol / Generic mfg.
Journal: Pathogenic role of innate immunity in a model of chronic NO inhibition associated with salt overload. (Pubmed Central) - Mar 31, 2020 Adult male Munich-Wistar rats that received l-NAME in drinking water with salt overload (HS + N group) were treated with allopurinol (ALLO) as an NLRP3 inhibitor (HS + N + ALLO group) or pyrrolidine dithiocarbamate (PDTC) as an NF-κB inhibitor (HS + N + PDTC group)...Overall, PDTC promoted a more efficient anti-inflammatory and nephroprotective effect than ALLO. The NLRP3/IL-1β and TLR4/NF-κB pathways act in parallel to promote renal injury/inflammation and must be simultaneously inhibited for best nephroprotection.
- |||||||||| Journal: NLRP3 Inflammasome Mediates White Adipose Tissue Browning After Burn. (Pubmed Central) - Mar 31, 2020
These results suggest that NLRP3 has anti-browning effects and that blocking NLRP3 increases thermogenesis and augments browning via increased levels of IL-6. Our findings provide insights into targeting innate inflammatory systems for regulation of adaptive thermogenesis, a critical response after burns and other hypermetabolic conditions.
- |||||||||| Journal: DDX3X acts as a live-or-die checkpoint in stressed cells by regulating NLRP3 inflammasome. (Pubmed Central) - Mar 31, 2020
Our findings suggest that macrophages use the availability of DDX3X to interpret stress signals and choose between pro-survival stress granules and pyroptotic ASC specks. Together, our data demonstrate the role of DDX3X in driving NLRP3 inflammasome and stress granule assembly, and suggest a rheostat-like mechanistic paradigm for regulating live-or-die cell-fate decisions under stress conditions.
- |||||||||| Preclinical, Journal: Dendrobium officinale polysaccharides protected against ethanol-induced acute liver injury in vivo and in vitro via the TLR4/NF-κB signaling pathway. (Pubmed Central) - Mar 31, 2020
In vitro experiments indicated that DOP increased the LO cell viability; prevented LDH release prominently; reduced the secretion of IL-1β, IL-6, and TNF-α; and reversed the expression of IL-1β, IL-6, TNF-α, caspase 1, NLRP3, p-NF-κB, and TLR4. Overall, DOP can alleviate ethanol-induced acute liver injury via the TLR4/NF-κB signaling pathway.
- |||||||||| Journal: Does glycaemic control modulate the impairment of NLRP3 inflammasome activation in type 2 diabetes? (Pubmed Central) - Mar 29, 2020
Our data also suggest negative correlations between HbA1c levels and NLRP3 protein expression, IL-12, caspase 1 and IL-1β mRNA expression. Our findings lead us to raise the hypothesis of an association between poor glycaemic control in T2D and an impairment of the NLRP3 inflammasome, suggesting that glycaemic control plays an important role in the immune response of diabetic subjects.
- |||||||||| Journal: Inflammasome and cytokine expression profiling in experimental periodontitis in the integrin β6 null mouse. (Pubmed Central) - Mar 29, 2020
Another significant difference between the Itgb6 and WT mice was that mRNA expression of the anti-inflammatory cytokine IL-10 was increased in ligatured WT mice but reduced in the Itgb6 mice. In conclusion, αvβ6 integrin in junctional epithelium of the gingiva appears to positively regulate the expression of the AIM2 inflammasome and anti-inflammatory IL-10, thus providing protection against periodontal inflammation.
- |||||||||| A-967079 / AbbVie
Journal: Roles of TRPA1 and TRPV1 in Cigarette Smoke -induced Airway Epithelial Cell Injury Model. (Pubmed Central) - Mar 29, 2020 Alveolar epithelial (A549) cells and bronchial epithelial (Beas-2B) cells were treated with CSE in the presence and absence of a TRPA1 inhibitor (100 μM, A967079), a TRPV1 inhibitor (100 μM, AMG9810) or both...They also prevented the changes in mitochondrial fission and fusion proteins and in MRC complexes activities induced by CSE. Both TRPA1 and TRPV1 mediate CSE-induced damage of airway and alveolar epithelial cells via modulation of oxidative stress, inflammation and mitochondrial damage and their inhibition should be considered as potential therapy for COPD.
- |||||||||| Preclinical, Journal: Macrophage β2-Integrins Regulate IL-22 by ILC3s and Protect from Lethal Citrobacter rodentium-Induced Colitis. (Pubmed Central) - Mar 29, 2020
β2-integrin expression on macrophages is mechanistically linked to Rac1/ROS-mediated induction of noncanonical-NLRP3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3) inflammasome-dependent IL-1β production, which promotes ILC3-derived IL-22. Therefore, β2-integrins are required for protective IL-1β-dependent IL-22 responses in colitis, and the identified mechanism may underlie the association of human LAD1 with colitis.
- |||||||||| Review, Journal: Methanogenic Archaea: Emerging Partners in the Field of Allergic Diseases. (Pubmed Central) - Mar 29, 2020
At the subcellular level, methanogenic Archaea are activators of the TLR8-dependent NLRP3 inflammasome, modulate the release of antimicrobial peptides and drive the production of proinflammatory, Th-1, Th-2, and Th-17 cytokines. Our objective was to introduce the most recent and major pieces of evidence supporting the involvement of Archaea in the balance between health and dysimmune diseases, with a particular focus on atopic and allergic conditions.
- |||||||||| Review, Journal: ER Stress Activates the NLRP3 Inflammasome: A Novel Mechanism of Atherosclerosis. (Pubmed Central) - Mar 29, 2020
Both ER stress and the NLRP3 inflammasome have emerged as critical individual contributors of AS, and owing to the multiple associations between these two events, we speculate that they contribute to the mechanisms of pathogenesis in AS. In this review, we aim to summarize the molecular mechanisms of ER stress, NLRP3 inflammasome activation, and the cross talk between these two pathways in AS in the hopes of providing new pharmacological targets for AS treatment.
- |||||||||| Review, Journal: Heme oxygenase-1/carbon monoxide as modulators of autophagy and inflammation. (Pubmed Central) - Mar 29, 2020
The interplay between mitochondrial autophagy, mitochondrial dysfunction, and the regulation and resolution of inflammation may make important contributions to the protection afforded by HO-1/CO in cellular and organ injury models. Recent studies have continued to explore the potential of CO for clinical applications.
- |||||||||| The Nod-Like Receptor Family, Pyrin-Containing 3 (NLRP3) a Biological Target for Mood Disorders () - Mar 25, 2020 - Abstract #ISBD2020ISBD_176;
It is critically important to understand whether the involvement of inflammasome activation happens in early years of development. Thus, providing novel biologically-based knowledge for disease classification in youth with a diagnosis of mood disorders (either BD or MDD), ultimately promoting better care for patients and use of different therapeutic strategies ultimately leading to a more efficient treatment and prevention of disease progression.
- |||||||||| Journal: Sirtuin regulation of NLRP3. (Pubmed Central) - Mar 25, 2020
The proceedings of this symposium may lead to some potential neuroinflammatory biomarkers and therapeutic targets for BD. No abstract available
- |||||||||| doxorubicin hydrochloride / Generic mfg.
Journal, IO Biomarker: Embryonic Stem Cell-Derived Exosomes Inhibit Doxorubicin Induced TLR4-NLRP3 Mediated Cell Death - Pyroptosis. (Pubmed Central) - Mar 24, 2020 Furthermore, our cytokine array data suggests increased anti-inflammatory (IL-4, IL-9 and IL-13) and decreased pro-inflammatory cytokines (Fas ligand, IL-12 and TNF-α) in ES-Exos, suggesting that anti-inflammatory cytokines might be mediating the protective effects of ES-Exos. In conclusion, our data shows that Dox induces pyroptotic cell death in the H9c2 cell culture model, and is attenuated via treatment with ES-Exos.
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