NLRP3 inhib 
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  • ||||||||||  Journal:  NEK7: a potential therapy target for NLRP3-related diseases. (Pubmed Central) -  Mar 16, 2021   
    Furthermore, NEK7 has been proved to be involved in many NLRP3-related diseases in humans or in animal models. Inhibitors focused on NEK7 may regulate NLRP3 to abolish the inflammation response and NEK7 may be a potential therapeutic target for NLRP3-related diseases.
  • ||||||||||  Journal:  Oxidative stress induced pyroptosis leads to osteogenic dysfunction of MG63 cells. (Pubmed Central) -  Mar 16, 2021   
    Further, inhibition of the NLRP3 inflammasome with MCC950 improved osteoblast migration and restored the expression of osteogenic differentiation-related proteins such as COL 1, RUNX 2 and ALP. In conclusion, oxidative stress caused by LPS induces pyroptosis in osteoblasts, leading to osteogenic dysfunction.
  • ||||||||||  Remicade (infliximab) / Mitsubishi Tanabe, J&J, Stelara (ustekinumab) / J&J, Humira (adalimumab) / Eisai, AbbVie
    Review, Journal:  Hidradenitis Suppurativa as a Potential Subtype of Autoinflammatory Keratinization Disease. (Pubmed Central) -  Mar 16, 2021   
    These findings collectively suggest that HS is closely linked with aberrant keratinization and autoinflammation, raising the question whether it represents an autoinflammatory keratinization disease, a recently proposed disease entity. In this mini review, I introduce the concept of autoinflammatory keratinization disease and attempt to address this clinically important question.
  • ||||||||||  Review, Journal:  Obesity, Nutrients and the Immune System in the Era of COVID-19. (Pubmed Central) -  Mar 16, 2021   
    Furthermore, in obese subjects, the already present endothelial dysfunction will render endothelial inflammation (endotheliitis) due to viral infiltration all the more severe. Added to this is a state of hypercoagulability and a decrease in respiratory capacity, leading to a risk of severe COVID-19 with cardiovascular complications, acute respiratory distress syndrome, and disseminated intravascular coagulation, which can lead to multiple organ failure and even death.
  • ||||||||||  Review, Journal:  Targeting the NLRP3 Inflammasome via BTK. (Pubmed Central) -  Mar 16, 2021   
    Furthermore, I review recent (pre-)clinical evidence for effects of BTK inhibitors on NLRP3 activity and highlight and discuss open questions and future research directions. Collectively, the concept of targeting BTK to target NLRP3-dependent inflammation will be explored comprehensively at the molecular, cellular and therapeutic levels.
  • ||||||||||  Journal:  SARS-CoV-2, SARS-CoV-1, and HIV-1 derived ssRNA sequences activate the NLRP3 inflammasome in human macrophages through a non-classical pathway. (Pubmed Central) -  Mar 16, 2021   
    Here, we show that GU-rich single-stranded RNA (GU-rich RNA) derived from SARS-CoV-2, SARS-CoV-1 and HIV-1 trigger a TLR8-dependent pro-inflammatory cytokine response from human macrophages in the absence of pyroptosis, with GU-rich RNA from the SARS-CoV-2 spike protein triggering the greatest inflammatory response. Using genetic and pharmacological inhibition, we show that the induction of mature IL-1β is through a non-classical pathway dependent upon caspase-1, caspase-8, the NLRP3 inflammasome, potassium efflux, and autophagy while being independent of TRIF (TICAM1), vitamin D3, and pyroptosis.
  • ||||||||||  [VIRTUAL] EXOME SEQUENCING IN 30,000 CASES DEFINES NOVEL RISK FACTORS FOR CROHN'S DISEASE (DDW Virtual) -  Mar 15, 2021 - Abstract #DDW2021DDW_1511;    
    28 variants already achieved exome-wide significance p<3x10-7 in the first analysis, including variants at genes from prior GWAS and sequencing efforts: NOD2, IL23R, LRRK2, TYK2, SLC39A8, HGFAC, IRGM and CARD9.After replication, coding variants in novel genes exceeding study-wise significance include genes related to pathogenic processes in IBD include DOK2:P274L (downstream of tyrosine kinase 2: myeloid cell development and negative regulator of TLR2), TAGAP:E147K (Th17 differentiation and antifungal signaling), PTAFR:N114S (regulates NLRP3 inflammasome), CCR7:M7V (homing of T cells and dendritic cells, lymphocyte egress, regulatory and memory T cell function), IL10RA:P295L (a VEOIBD gene, regulator of innate/adaptive immune responses), RELA:D288N (Th17 regulator and AD chronic mucocutaneous ulceration) as well as variants at PDLIM5, INSC and SDF2L1.ConclusionThese findings provide novel launch points for mechanistic studies that will further our understanding of disease pathogenesis. For example, SDF2L1 (R161H) flags a gene not previously implicated in IBD but which is reported to regulate feeding-induced ER stress, with a series of CRISPR screens identifying it as an essential regulator of ER homeostasis.
  • ||||||||||  [VIRTUAL] Extracellular Specks, a Marker of NLRP3 Inflammasome Activation () -  Mar 14, 2021 - Abstract #ATS2021ATS_4506;    
    We evaluated an commercially available antibody for use in the detection of eSpecks. Further work using patient material is necessary to evaluate the usefulness of this approach to detect activation of NLRP3 inflammasome.
  • ||||||||||  [VIRTUAL] Novel Pharmacodynamic Model to Profile Inhibitors of NLRP3 in the Mouse Lung () -  Mar 14, 2021 - Abstract #ATS2021ATS_2696;    
    We have developed an acute in vivo model to help study the effect of NLRP3 inhibitors in the airways. This short mechanistic model will serve as an invaluable tool in the development of modulators of the NLRP3 inflammasome and will help with the drive to finding novel therapies for chronic lung diseases.
  • ||||||||||  montelukast / Generic mfg.
    [VIRTUAL] Genome-Wide Association Study for Longitudinal Therapeutic Response to Montelukast in Adults with Asthma () -  Mar 14, 2021 - Abstract #ATS2021ATS_2635;    
    Notably, SNP rs10925023 (P=2.8E-06) annotated to NLRP3 which plays a role in the regulation of inflammation in asthma. Replication of the top 213 SNPs in the Mass General Brigham Biobank is underway.CONCLUSIONSThrough a discovery GWAS for the association of asthma exacerbation rate following treatment with montelukast, we identified 213 SNPs that are approaching genome-wide significance to test in a replication cohort.
  • ||||||||||  [VIRTUAL] Different Doses of LPS Affect Macrophage Polarization and Alter the Asthma Phenotype () -  Mar 14, 2021 - Abstract #ATS2021ATS_38;    
    In closer examination of IMs, M1 (CD86+CD206-) increased more in OH compared to OL whereas, M2 (CD86-CD206+) increased equally in both of OL and OH. CD86+CD206+ IMs, which showed good correlation with Th17, also increased in LPS dose-dependent fashion.Conclusion Macrophage polarization by different doses of LPS may play a key role in determining Th2/Th17 balance which result in distinct immunologic phenotypes of asthma.
  • ||||||||||  Preclinical, Journal:  Vimentin regulation of autophagy activation in lung fibroblasts in response to lipopolysaccharide exposure in vitro. (Pubmed Central) -  Mar 13, 2021   
    Importantly, the mechanism of suppression of vimentin in the lung fibroblasts was caused by a decrease in autophagy, an increase in mitochondrial membrane protein, and a decrease in mitochondrial function, which may contribute to the augmented cellular injury generated during the response to LPS. This study provides insights into whether vimentin may interfere with the inflammatory cascade by activating the autophagy pathway of mitochondrial lung fibroblasts in the early stage of acute lung injury (ALI).
  • ||||||||||  risperidone / Generic mfg., clozapine / Generic mfg.
    Journal:  Clozapine Prevents Poly (I:C) Induced Inflammation by Modulating NLRP3 Pathway in Microglial Cells. (Pubmed Central) -  Mar 12, 2021   
    Clozapine reduced the level of poly (I:C)-activated NLRP3 expression by 57%, which was higher than the reduction thay was seen with CRID3 treatment (45%). These results suggest that clozapine might exhibit anti-inflammatory effects by inhibiting NLRP3 inflammasome and this activity is not typical with the use of other antipsychotic drugs under the conditions of strong microglial activation.
  • ||||||||||  Preclinical, Journal:  Cinnamaldehyde suppresses NLRP3 derived IL-1β via activating succinate/HIF-1 in rheumatoid arthritis rats. (Pubmed Central) -  Mar 12, 2021   
    In addition, CA also inhibited the expression of the succinate receptor GPR91, which in turn inhibited the activation of HIF-1α. In conclusions, our results suggested that CA might be a potential therapeutic compound to relieve rheumatoid arthritis progress by suppressing IL-1β through modulating succinate/HIF-1α axis and inhibition of NLRP3.
  • ||||||||||  Preclinical, Journal:  Requirement of Complement C6 for Intact Innate Immune Responses in Mice. (Pubmed Central) -  Mar 12, 2021   
    In a model of acute lung injury induced by LPS, C6 mice showed reduced PMN buildup and less lung epithelial/endothelial cell dysfunction (edema and hemorrhage). These data indicate that C6 mice have reduced innate immune responses that result in less organ injury and improved survival after polymicrobial sepsis.
  • ||||||||||  Journal:  Lipopolysaccharide-induced DC-SIGN/TLR4 crosstalk activates NLRP3 inflammasomes via MyD88-independent signaling in gastric epithelial cells. (Pubmed Central) -  Mar 12, 2021   
    The results of flow cytometry analysis show that DC-SIGN primarily mediates Th1 differentiation when co-cultured with gastric epithelial cells. These results reveal that LPS-induced DC-SIGN expression modulates NLRP3 inflammasomes formation via MyD88-independent TLR4 signaling in gastric epithelial cell, and induces a Th1-predominant host immune response,these findings may indicate a new function of DC-SIGN in non-immune cells, and elucidate the diversity role of gastric epithelial cells in mechanism of immune damage caused by microbial flora.
  • ||||||||||  Journal:  DNA Damage Promotes Epithelial Hyperplasia and Fate Mis-specification via Fibroblast Inflammasome Activation. (Pubmed Central) -  Mar 12, 2021   
    Instead, dermal fibroblasts are both necessary and sufficient to induce the epithelial response, which is mediated by activation of a fibroblast-specific NLRP3 inflammasome and subsequent IL-1β production. Thus, genotoxic agents that are used chemotherapeutically to promote cancer cell death can have the opposite effect on wild-type epithelia by inducing, via a non-autonomous IL-1β-driven mechanism, both hyperplasia and stem cell lineage defects.
  • ||||||||||  Journal:  Parsing the IL-37-Mediated Suppression of Inflammasome Function. (Pubmed Central) -  Mar 11, 2021   
    In mice subjected to endotoxemia, IL-37 inhibited plasma IL-1β (-78% compared to wild-type animals) and IL-18 (-61%). Thus, our study adds suppression of inflammasome activity to the portfolio of anti-inflammatory pathways employed by IL-37, highlighting this cytokine as a potential tool for treating inflammasome-driven diseases.