1-ethyl-3-(6-methylphenanthridine-8-il) urea modulates TLR3/9 activation and induces selective pro-inflammatory cytokine expression in vitro

2017 ◽  
Vol 27 (7) ◽  
pp. 1530-1537 ◽  
Author(s):  
Natalija Knežević Teofilović ◽  
Mahjoub Bihi ◽  
Marijana Radić Stojković ◽  
Lidija M. Tumir ◽  
Katja Ester ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Cytokine Expression

scholarly journals SOCS1/SOCS3 Immune Axis Modulates Synthetic Perturbations in IL6 Biological Circuit for Dynamical Cellular Response

2020 ◽  
Author(s):  
Bhavnita Soni ◽  
Shailza Singh
Keyword(s):  
Signaling Pathway ◽  
Cellular Response ◽  
Inflammatory Cytokine ◽  
Cytokine Expression ◽  
Janus Kinase ◽  
Cytokine Signaling ◽  
Macrophage Phenotype ◽  
Regulatory Circuit ◽  
Stat Pathway

AbstractMacrophage phenotype plays a crucial role in the pathogenesis of Leishmanial infection. Pro-inflammatory cytokines are the key regulators that eliminate the infection induced by Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. Suppressor of cytokine signaling (SOCS) is a well-known negative feedback regulator of JAK/STAT pathway. However, change in expression levels of SOCS in correlation with the establishment of infection is not well understood. Mathematical modeling of IL6 signaling pathway have helped identified the role of SOCS1 in establishment of infection. Furthermore, the ratio of SOCS1 and SOCS3 has been quantified both in silico as well as in vitro, indicating an immune axis which governs the macrophage phenotype during L. major infection. The ability of SOCS1 protein to inhibit the JAK/STAT1 signaling pathway and thereby decreasing pro-inflammatory cytokine expression makes it a strong candidate for therapeutic intervention. Using synthetic biology approaches, peptide based immuno-regulatory circuit have been designed to target the activity of SOCS1 which can restore pro-inflammatory cytokine expression during infection.

scholarly journals Sophorolipid treatment decreases inflammatory cytokine expression in an in vitro model of experimental sepsis

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Cathy M Mueller ◽  
Yin‐yao Lin ◽  
Domenico Viterbo ◽  
Joelle Pierre ◽  
Shirley A Murray ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
In Vitro Model ◽  
Cytokine Expression ◽  
Experimental Sepsis ◽  
Vitro Model

Effect of peiminine on DNCB-induced atopic dermatitis by inhibiting inflammatory cytokine expression in vivo and in vitro

2018 ◽  
Vol 56 ◽  
pp. 135-142 ◽  
Author(s):  
Jeong-Min Lim ◽  
Bina Lee ◽  
Ju-Hee Min ◽  
Eun-Young Kim ◽  
Jae-Hyun Kim ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Inflammatory Cytokine ◽  
Cytokine Expression

scholarly journals Characterization of Pathogenesis and Inflammatory Responses to Experimental Parechovirus Encephalitis

2021 ◽  
Vol 12 ◽  
Author(s):  
Ming-Wei Jan ◽  
Hong-Lin Su ◽  
Tsung-Hsien Chang ◽  
Kuen-Jer Tsai
Keyword(s):  
Mouse Brain ◽  
Inflammatory Cytokine ◽  
Inflammatory Responses ◽  
Disease Model ◽  
Clinical Manifestations ◽  
Cytokine Expression ◽  
Etiologic Factor ◽  
Neuronal System ◽  
Cytopathic Effects

Human parechovirus type 3 (PeV-A3) infection has been recognized as an emerging etiologic factor causing severe nerve disease or sepsis in infants and young children. But the neuropathogenic mechanisms of PeV-A3 remain unknown. To understand the pathogenesis of PeV-A3 infection in the neuronal system, PeV-A3-mediated cytopathic effects were analyzed in human glioblastoma cells and neuroblastoma cells. PeV-A3 induced interferons and inflammatory cytokine expression in these neuronal cells. The pronounced cytopathic effects accompanied with activation of death signaling pathways of apoptosis, autophagy, and pyroptosis were detected. A new experimental disease model of parechovirus encephalitis was established. In the disease model, intracranial inoculation with PeV-A3 in C57BL/6 neonatal mice showed body weight loss, hindlimb paralysis, and approximately 20% mortality. PeV-A3 infection in the hippocampus and cortex regions of the neonatal mouse brain was revealed. Mechanistic assay supported the in vitro results, indicating detection of PeV-A3 replication, inflammatory cytokine expression, and death signaling transduction in mouse brain tissues. These in vitro and in vivo studies revealed that the activation of death signaling and inflammation responses is involved in PeV-A3-mediated neurological disorders. The present results might account for some of the PeV-A3-associated clinical manifestations.

scholarly journals Long noncoding RNA GSEC promotes neutrophil inflammatory activation by supporting PFKFB3-involved glycolytic metabolism in sepsis

2021 ◽  
Vol 12 (12) ◽  
Author(s):  
Dadong Liu ◽  
Wen Sun ◽  
Danying Zhang ◽  
Zongying Yu ◽  
Weiting Qin ◽  
...  
Keyword(s):  
Noncoding Rna ◽  
Inflammatory Cytokine ◽  
Process Analysis ◽  
Expression Patterns ◽  
Cytokine Expression ◽  
Neutrophil Activation ◽  
Metabolic Reprogramming ◽  
Glycolytic Metabolism ◽  
Inflammatory Activation

AbstractMetabolic reprogramming is a hallmark of neutrophil activation in sepsis. LncRNAs play important roles in manipulating cell metabolism; however, their specific involvement in neutrophil activation in sepsis remains unclear. Here we found that 11 lncRNAs and 105 mRNAs were differentially expressed in three transcriptome datasets (GSE13904, GSE28750, and GSE64457) of gene expression in blood leukocytes and neutrophils of septic patients and healthy volunteers. After Gene Ontology biological process analysis and lncRNA–mRNA pathway network construction, we noticed that GSEC lncRNA and PFKFB3 were co-expressed and associated with enhanced glycolytic metabolism. Our clinical observations confirmed the expression patterns of GSEC lncRNA and PFKFB3 genes in neutrophils in septic patients. Performing in vitro experiments, we found that the expression of GSEC lncRNA and PFKFB3 was increased when neutrophils were treated with inflammatory stimuli. Knockdown and overexpression experiments showed that GSEC lncRNA was essential for mediating PFKFB3 mRNA expression and stability in neutrophil-like dHL-60 cells. In addition, we found that GSEC lncRNA-induced PFKFB3 expression was essential for mediating dHL-60 cell inflammatory cytokine expression. Performing mechanistic experiments, we found that glycolytic metabolism with PFKFB3 involvement supported inflammatory cytokine expression. In summary, our study uncovers a mechanism by which GSEC lncRNA promotes neutrophil inflammatory activation in sepsis by supporting glycolytic metabolism with PFKFB3.

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