NLRP3 inhib 
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  • ||||||||||  Journal:  Macrophage priming is dispensable for NLRP3 inflammasome activation and restriction of Leishmania amazonensis replication. (Pubmed Central) -  May 27, 2020   
    By contrast, BMDM priming was required for CASP1 cleavage (p20) and IL-1β secretion, because priming triggers robust up-regulation of pro-IL-1β and CASP11 that are important for efficient processing of CASP1 and IL-1β. Taken together, our data shed light into the cellular and molecular processes involved in activation of the NLRP3 in macrophages by Leishmania, a process that is important for the outcome of Leishmaniasis.
  • ||||||||||  Journal:  Activation of ROS/MAPKs/NF-κB/NLRP3 and inhibition of efferocytosis in osteoclast-mediated diabetic osteoporosis. (Pubmed Central) -  May 27, 2020   
    In streptozotocin-induced diabetic rats in vivo, the numbers and the bone-resorption capacity of OCs as well as the serum levels of TRACP-5b were significantly increased, and the expression of MAPK-, NF-κB-, and NLRP3 inflammasome-related proteins in the proximal tibia were also significantly elevated; however, treatment with insulin and LXA4 reversed this elevation. Together, these results demonstrated that the activation of ROS/MAPKs/NF-κB/NLRP3 and the inhibition of efferocytosis in OCs are the main causes of osteoporosis in DM.-An, Y., Zhang, H., Wang, C., Jiao, F., Xu, H., Wang, X., Luan, W., Ma, F., Ni, L., Tang, X., Liu, M., Guo, W., Yu, L. Activation of ROS/MAPKs/NF-κB/NLRP3 and inhibition of efferocytosis in osteoclast-mediated diabetic osteoporosis.
  • ||||||||||  colchicine / Generic mfg.
    Journal:  Colchicine inhibits endothelial inflammation via NLRP3/CRP pathway. (Pubmed Central) -  May 26, 2020   
    In summary, SAC can protect liver against LPS/d-Gal by attenuation of neutrophil infiltration, oxidative stress, inflammation, apoptosis, and pyroptosis which is partly linked to its suppression of TLR4/NF-κB/NLRP3 signaling. No abstract available
  • ||||||||||  tamoxifen / Generic mfg.
    Preclinical, Journal:  NLRP3 inflammasome activation in hepatic stellate cells induces murine liver fibrosis. (Pubmed Central) -  May 23, 2020   
    Primary HSCs isolated from wild-type (WT), Nlrp3 , or Nlrp3 knock-in crossed to inducible (estrogen receptor Cre-CreT) mice were incubated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP), or 4OH-tamoxifen, respectively...Liver sections from 24 week-old Nlrp Lrat Cre mice showed fibrotic changes with increased αSMA and desmin positive cells and collagen deposition, independent of inflammatory infiltrates; these changes were also observed after LPS challenge in 8 week-old Nlrp Lrat Cre mice. Conclusion Our results highlight a direct role for the NLRP3 inflammasome in the activation of HSC directly triggering liver fibrosis.
  • ||||||||||  Review, Journal:  Reactive species-induced microvascular dysfunction in ischemia/reperfusion. (Pubmed Central) -  May 23, 2020   
    On the other hand, RS production at signaling levels promotes ischemic angiogenesis, mediates flow-induced dilation in patients with coronary artery disease, and instigates the activation of cell survival programs by conditioning stimuli that render tissues resistant to the deleterious effects of prolonged I/R. These topics will be reviewed in this article.
  • ||||||||||  Decadron (dexamethasone) / Merck (MSD)
    Journal:  Contribution of cathepsin B-dependent Nlrp3 inflammasome activation to nicotine-induced endothelial barrier dysfunction. (Pubmed Central) -  May 23, 2020   
    Collectively, our data suggest that nicotine enhances cathepsin B-dependent Nlrp3 inflammasome activation and the consequent production of a novel permeability factor HMGB1, which causes disruption of inter-endothelial tight junctions leading to endothelial hyperpermeability. Instigation of endothelial inflammasomes may serve as an important pathogenic mechanism contributing to the early onset of vasculopathy associated with smoking.
  • ||||||||||  Actemra IV (tocilizumab) / Roche, JW Pharma, Kineret (anakinra) / SOBI, Affibody
    [VIRTUAL] EFFICACY OF ANAKINRA TREATMENT IN PEDIATRIC RHEUMATIC DISEASES; A SINGLE-CENTER EXPERIENCE () -  May 22, 2020 - Abstract #EULAR2020EULAR_4011;    
    Anakinra seems to be a successful treatment to achieve inactive disease in a significant portion of patients in the early period. The recurrence of disease attacks while drug tapering and injection site reactions were appears the main causes of treatment switch or discontinuation.
  • ||||||||||  colchicine / Generic mfg., Ilaris (canakinumab) / Novartis
    [VIRTUAL] CLINICAL FEATURES AND ANALYSIS OF MEFV GENE IN 31 PATIENTS WITH FAMILIAL MEDITERRANEAN FEVER (FMF) () -  May 22, 2020 - Abstract #EULAR2020EULAR_3227;    
    We have examined association between clinical features and mutations of MEFV in 31 patients in Gifu district, suggesting that duration of fever attacks and frequency of fever attacks in G1 are significantly shorter than G2 and G3, respectively in Japanese patients with FMF. Mutations of E148Q in exon 2 were observed in 16-23 % of normal Japanese patients, indicating that E148Q is the polymorphism or accelerating factor.
  • ||||||||||  lenabasum (JBT-101) / Corbus Pharma, Kaken
    [VIRTUAL] LENABASUM, A CB2 AGONIST, INHIBITS INFLAMMASOME ACTIVATION () -  May 22, 2020 - Abstract #EULAR2020EULAR_1633;    
    Our data revealed that Ala 348 to Thr up-regulate the functional status of P2X7R and Glu 496 to Ala and Gln 460 to Arg down-regulate the functional status of P2X7R, which resulted in a significant increase or decrease in IL-1β and NLRP3 expression levels with high uric acid. Lenabasum inhibits inflammasome activation, which could contribute to potential therapeutic efficacy in SSc and other autoimmune diseases.
  • ||||||||||  Journal:  Design, synthesis, and screening of sulfonylurea-derived NLRP3 inflammasome inhibitors. (Pubmed Central) -  May 22, 2020   
    The polar enone functional alert of chalcone was replaced with a sulfonylurea scaffold while maintaining the relative positions of the two aromatic rings. These compounds were evaluated for their ability to inhibit NLRP3 and AIM2 inflammasome activation triggered by Francisella tularensis infection.
  • ||||||||||  low molecular weight dextran sulfate (ILB) / TikoMed
    Journal:  Caffeic Acid Phenethyl Ester Prevents Colitis-Associated Cancer by Inhibiting NLRP3 Inflammasome. (Pubmed Central) -  May 22, 2020   
    Here, we aimed to evaluate the anti-inflammatory effect of caffeic acid phenethyl ester (CAPE) on bone marrow-derived macrophages (BMDMs), THP-1 cells, and azoxymethane/dextran sulfate sodium (AOM/DSS)-induced colon cancer mouse model...Altogether, our findings demonstrate that CAPE prevents CAC by post-transcriptionally inhibiting NLRP3 inflammasome. Thus, CAPE may be an effective candidate for reducing the risk of CAC in patients with inflammatory bowel disease.
  • ||||||||||  Journal:  Zearalenone induces NLRP3-dependent pyroptosis via activation of NF-κB modulated by autophagy in INS-1 cells. (Pubmed Central) -  May 21, 2020   
    Furthermore, we indicated that ZEA-induced NF-κB p65 activation contributed to the activation of the NLRP3 inflammasome, inflammatory response, and pyroptosis in INS-1 cells, which were indicated by western blot and immunofluorescence, and the activation of NF-κB p65 induced by ZEA was autophagy-dependent. This study demonstrates that ZEA induces NLRP3-dependent pyroptosis via activation of NF-κB modulated by autophagy in INS-1 cells.
  • ||||||||||  [VIRTUAL] Non Targeting Locked Nucleic Acids Antagonize Inflammatory Activation of Foam Cells and Impede Atherosclerosis () -  May 20, 2020 - Abstract #ATVBPVDGPM2020ATVB_PVD_GPM_103;    
    Moreover, differential expression analysis of leukocyte populations revealed blunted expression of inflammatory mediators (Il1b, Nlrp3, Tnf), oxidative stress (Mpo, Sod2, Ptgs2), and extracellular matrix remodeling genes (Mmp9, Prtn3, Elane). Taken together, our results put forth a novel paradigm in which sRNA-cargo of LDL promote inflammatory activation of macrophages in the artery wall and identify TLR8 antagonism with ntLNA as a viable strategy for the treatment of chronic inflammation in CVD.