Toll‐like receptor 4 polymorphisms were associated with low serum pro‐inflammatory cytokines in BCG osteitis survivors

2019 ◽  
Vol 109 (7) ◽  
pp. 1417-1422 ◽  
Author(s):  
Matti Korppi ◽  
Johanna Teräsjärvi ◽  
Eero Lauhkonen ◽  
Heini Huhtala ◽  
Kirsi Nuolivirta ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Low Serum ◽  
Pro Inflammatory Cytokines

Effects of local lipopolysaccharide administration on the expression of Toll-like receptor 4 and pro-inflammatory cytokines in uterus and oviduct of rabbit does

2018 ◽  
Vol 107 ◽  
pp. 162-174 ◽  
Author(s):  
Laura Menchetti ◽  
Olimpia Barbato ◽  
Iulia Elena Filipescu ◽  
Giovanna Traina ◽  
Leonardo Leonardi ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Pro Inflammatory Cytokines

scholarly journals Effects of Adipose-Derived Biogenic Nanoparticle-Associated microRNA-451a on Toll-like Receptor 4-Induced Cytokines

Pharmaceutics ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 16
Author(s):  
Xinghua Wang ◽  
Anthony Pham ◽  
Lu Kang ◽  
Sierra A. Walker ◽  
Irina Davidovich ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Signaling Pathways ◽  
Extracellular Vesicles ◽  
Inflammatory Cytokines ◽  
Stromal Cells ◽  
Toll Like Receptor ◽  
Immunomodulatory Effects ◽  
Toll Like Receptor 4 ◽  
Biogenic Nanoparticles ◽  
Pro Inflammatory Cytokines

Extracellular vesicles (EVs) are cell-released nanoparticles that transfer biomolecular content between cells. Among EV-associated biomolecules, microRNAs (miRNAs/miRs) represent one of the most important modulators of signaling pathways in recipient cells. Previous studies have shown that EVs from adipose-derived mesenchymal stromal cells (MSCs) and adipose tissue modulate inflammatory pathways in macrophages. In this study, the effects of miRNAs that are abundant in adipose tissue EVs and other biogenic nanoparticles (BiNPs) were assessed in terms of altering Toll-like receptor 4 (TLR4)-induced cytokines. TLR-4 signaling in macrophages is often triggered by pathogen or damage-induced inflammation and is associated with several diseases. This study demonstrates that miR-451a, which is abundant in adipose tissue BiNPs, suppresses pro-inflammatory cytokines and increases anti-inflammatory cytokines associated with the TLR4 pathway. Therefore, miR-451a may be partially responsible for immunomodulatory effects of adipose tissue-derived BiNPs.

scholarly journals Soluble CD14 Induces Pro-inflammatory Cytokines in Rheumatoid Arthritis Fibroblast-Like Synovial Cells via Toll-Like Receptor 4

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1689
Author(s):  
Yoshihide Ichise ◽  
Jun Saegusa ◽  
Shino Tanaka-Natsui ◽  
Ikuko Naka ◽  
Shinya Hayashi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Inflammatory Cytokines ◽  
Intercellular Adhesion Molecule ◽  
Toll Like Receptor ◽  
Intercellular Adhesion Molecule 1 ◽  
Toll Like Receptor 4 ◽  
Soluble Cd14 ◽  
Mrna Induction ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Objectives: Synovial fluids of rheumatoid arthritis (RA) patients commonly contain high concentrations of soluble CD14 (sCD14). To investigate its potential role in RA pathogenesis, we tested whether sCD14 binding transmits a signal to fibroblast-like synoviocytes from RA patients (RA-FLS). Methods: The induction of pro-inflammatory cytokines, chemokines, and mediators by sCD14 stimulation of RA-FLS was quantified by real-time PCR and ELISA. Cell proliferation was assessed by the BrdU assay. LPS-RS, a Toll-like receptor 4 (TLR-4) antagonist, was used to block TLR-4 signaling. Results: Soluble CD14 induced the expression of IL-6 mRNA and secretion of the protein. The expression of other pro-inflammatory cytokines and mediators, such as TNF-α, IL-8, intercellular adhesion molecule-1 (ICAM-1), MMP-3, and RANK ligand (RANKL), was also induced by sCD14. In addition, sCD14 stimulation promoted RA-FLS proliferation. LPS-RS abolished IL-6, IL-8, and ICAM-1 mRNA induction by sCD14 in RA-FLS. On the other hand, TNF-α and IL-17A increased TLR-4 expression by RA-FLS and amplified their sCD14-induced IL-6 expression. Conclusions: Soluble CD14 transmits inflammatory signals to RA-FLS via TLR-4. The effects of sCD14 may be augmented in inflammatory milieu. Our results suggest that sCD14 is involved in the pathogenesis of RA and may be a novel therapeutic target.

scholarly journals A Human Anti-Toll Like Receptor 4 Fab Fragment Inhibits Lipopolysaccharide-Induced Pro-Inflammatory Cytokines Production in Macrophages

PLoS ONE ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. e0146856 ◽  
Author(s):  
Maorong Wang ◽  
Wenkai Zheng ◽  
Xuhui Zhu ◽  
Jing Xu ◽  
Binggang Cai ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Toll Like Receptor ◽  
Fab Fragment ◽  
Toll Like Receptor 4 ◽  
Pro Inflammatory Cytokines

scholarly journals Predominant phosphorylation patterns in Neisseria meningitidis lipid A determined by top-down MS/MS

2020 ◽  
Vol 61 (11) ◽  
pp. 1437-1449
Author(s):  
Constance M. John ◽  
Nancy J. Phillips ◽  
Gary A. Jarvis
Keyword(s):  
Inflammatory Cytokines ◽  
Ion Mobility ◽  
Posttranslational Modifications ◽  
Lipid A ◽  
Molecular Ions ◽  
Innate Immune ◽  
Toll Like Receptor 4 ◽  
Adaptive Immune ◽  
Phosphoryl Groups ◽  
Pro Inflammatory Cytokines

Among the virulence factors in Neisseria infections, a major inducer of inflammatory cytokines is the lipooligosaccharide (LOS). The activation of NF-κB via extracellular binding of LOS or lipopolysaccharide (LPS) to the toll-like receptor 4 and its coreceptor, MD-2, results in production of pro-inflammatory cytokines that initiate adaptive immune responses. LOS can also be absorbed by cells and activate intracellular inflammasomes, causing the release of inflammatory cytokines and pyroptosis. Studies of LOS and LPS have shown that their inflammatory potential is highly dependent on lipid A phosphorylation and acylation, but little is known on the location and pattern of these posttranslational modifications. Herein, we report on the localization of phosphoryl groups on phosphorylated meningococcal lipid A, which has two to three phosphate and zero to two phosphoethanolamine substituents. Intact LOS with symmetrical hexa-acylated and asymmetrical penta-acylated lipid A moieties was subjected to high-resolution ion mobility spectrometry MALDI-TOF MS. LOS molecular ions readily underwent in-source decay to give fragments of the oligosaccharide and lipid A formed by cleavage of the ketosidic linkage, which enabled performing MS/MS (pseudo-MS3). The resulting spectra revealed several patterns of phosphoryl substitution on lipid A, with certain species predominating. The extent of phosphoryl substitution, particularly phosphoethanolaminylation, on the 4′-hydroxyl was greater than that on the 1-hydroxyl. The heretofore unrecognized phosphorylation patterns of lipid A of meningococcal LOS that we detected are likely determinants of both pathogenicity and the ability of the bacteria to evade the innate immune system.

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