scholarly journals Swine IRF3/IRF7 attenuates inflammatory responses through TLR4 signaling pathway

Oncotarget ◽  
2017 ◽  
Vol 8 (37) ◽  
pp. 61958-61968 ◽  
Author(s):  
Pei-Ge Chen ◽  
Yan-Jing Guan ◽  
Guang-Ming Zha ◽  
Xian-Qin Jiao ◽  
He-Shui Zhu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Inflammatory Responses ◽  
Tlr4 Signaling ◽  
Tlr4 Signaling Pathway

scholarly journals Dietary Silk Peptide Inhibits LPS-Induced Inflammatory Responses by Modulating Toll-Like Receptor 4 (TLR4) Signaling

Biomolecules ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 771
Author(s):  
Sungwoo Chei ◽  
Hyun-Ji Oh ◽  
Kippeum Lee ◽  
Heegu Jin ◽  
Jeong-Yong Lee ◽  
...  
Keyword(s):  
Immune Responses ◽  
Signaling Pathway ◽  
Inflammatory Responses ◽  
Innate Immune Responses ◽  
Toll Like Receptor ◽  
Serum Samples ◽  
Toll Like Receptor 4 ◽  
Tlr4 Signaling ◽  
Tlr4 Signaling Pathway ◽  
Silk Peptide

Acid-hydrolyzed silk peptide (SP) is a valuable material that has been used traditionally to treat various diseases, however, the mechanism by which it affects inflammatory responses is unknown. To examine the effects of SP on inflammatory responses, we used macrophages as a vehicle for examining signaling via toll-like receptor 4 (TLR4), which plays an important role in innate immune responses to pathogenic infections and pathogen-derived molecules such as lipopolysaccharide (LPS). We then confirmed the anti-inflammatory effects of SP by examining lymph node, spleen, and serum samples from C57BL/6 mice injected with LPS. We also used LPS-induced bone marrow-derived macrophages and RAW264.7 cells (a murine macrophage cell line) to identify the mechanism by which SP modulates immune responses via the TLR4 signaling pathway. In addition, we showed that SP prevents LPS-induced production of nitric oxide and reactive oxygen species. In summary, SP inhibits LPS-induced inflammatory responses by modulating the TLR4 signaling pathway.

Geniposide Reduces Inflammatory Responses of Oxygen-Glucose Deprived Rat Microglial Cells via Inhibition of the TLR4 Signaling Pathway

2012 ◽  
Vol 37 (10) ◽  
pp. 2235-2248 ◽  
Author(s):  
Jun Wang ◽  
Jincan Hou ◽  
Peng Zhang ◽  
Dan Li ◽  
Cuixiang Zhang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Inflammatory Responses ◽  
Microglial Cells ◽  
Tlr4 Signaling ◽  
Tlr4 Signaling Pathway

scholarly journals TLR4-Mediated Blunting of Inflammatory Responses to Eccentric Exercise in Young Women

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Rodrigo Fernandez-Gonzalo ◽  
José A. De Paz ◽  
Paula Rodriguez-Miguelez ◽  
María J. Cuevas ◽  
Javier González-Gallego
Keyword(s):  
Inflammatory Response ◽  
Training Program ◽  
Signaling Pathway ◽  
Young Women ◽  
Eccentric Exercise ◽  
Inflammatory Responses ◽  
Control Group ◽  
Eccentric Training ◽  
Tlr4 Signaling ◽  
Tlr4 Signaling Pathway

This study assessed the inflammatory response mediated by the toll-like receptor 4 (TLR4) signaling pathway after acute eccentric exercise before and after an eccentric training program in women. Twenty women performed two acute eccentric bouts using a squat machine over a ~9 week interval. The training group (TG) carried out an eccentric training program during 6 weeks, while the control group (CG) did not follow any training. Protein content of markers involved in the TLR4-mediated activation of several nuclear transcription factors, such as nuclear factorκB (NF-κB), and interferon regulatory transcription factor 3 (IRF3), was analyzed. The inflammatory response after the first acute bout was similar between TG and CG, showing an upregulation of all the markers analyzed, with the exception of IRF3. After the second bout, the upregulation of TLR4 signaling pathway was blunted in TG, but not in CG, through both the myeloid differentiation factor 88- and toll/interleukin-1 receptor domain containing adapter inducing interferon-β-dependent pathways. These results highlight the role of the TLR4 in controlling the exercise-induced inflammatory response in young women. More importantly, these data suggest eccentric training may help to prevent TLR4 activation principally through NF-κB, and perhaps IRF3, downstream signaling in this population.

scholarly journals Remote ischemic per-conditioning protects against renal ischemia–reperfusion injury via suppressing gene expression of TLR4 and TNF-α in rat model

2019 ◽  
Vol 97 (2) ◽  
pp. 112-119 ◽  
Author(s):  
Firouzeh Gholampour ◽  
Jamshid Roozbeh ◽  
Sahar Janfeshan ◽  
Zeinab Karimi
Keyword(s):  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Antioxidant Systems ◽  
Tlr4 Signaling ◽  
Tnf Α ◽  
Renal Ischemia Reperfusion Injury ◽  
Tlr4 Signaling Pathway

The pathogenesis of renal ischemia–reperfusion injury (IRI) involves both inflammatory processes and oxidative stress in the kidney. This study determined whether remote ischemic per-conditioning (RIPerC) is mediated by toll-like receptor 4 (TLR4) signaling pathway in rats. Renal IR injury was induced by occluding renal arteries for 45 min followed by 24 h of reperfusion. RIPerC included 4 cycles of 2 min of ischemia of the left femoral artery followed by 3 min of reperfusion performed at the start of renal ischemia. Rats were divided into sham, IR, and RIPerC groups. At the end of the reperfusion period, urine, blood and tissue samples were gathered. IR created kidney dysfunction, as ascertained by a significant decrease in creatinine clearance and a significant increase in sodium fractional excretion. These changes occurred in concert with a decrease in the activities of glutathione peroxidase, catalase, and superoxide dismutase with an increment in malondialdehyde levels, mRNA expression levels of TLR4 and tumor necrosis factor α (TNF-α), and histological damage in renal tissues. RIPerC treatment diminished all these changes. This study demonstrates that RIPerC has protective effects on the kidney after renal IR, which might be related to the inhibition of the TLR4 signaling pathway and augmentation of antioxidant systems.

scholarly journals The Absence of TLR4 Prevents Fetal Brain Injury in the Setting of Intrauterine Inflammation

2018 ◽  
Vol 26 (8) ◽  
pp. 1082-1093 ◽  
Author(s):  
Natalia M. Tulina ◽  
Amy G. Brown ◽  
Guillermo O. Barila ◽  
Michal A. Elovitz
Keyword(s):  
Brain Injury ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Quantitative Polymerase Chain Reaction ◽  
Fetal Brain ◽  
Notch Signaling Pathway ◽  
Mouse Strains ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tlr4 Signaling ◽  
Tlr4 Signaling Pathway

Background: Exposure to intrauterine inflammation during pregnancy is linked to brain injury and neurobehavioral disorders in affected children. Innate immunity, specifically Toll-like receptor (TLR) signaling pathways are present throughout the reproductive tract as well as in the placenta, fetal membranes, and fetus. The TLR pathways are mechanistically involved in host responses to foreign pathogens and may lead to brain injury associated with prenatal inflammation. Objective: We aimed to determine whether the activation of the TLR4 signaling pathway, in the mother and fetus, is critical to fetal brain injury in the setting of intrauterine inflammation. Methods: A mini-laparotomy was performed on time pregnant C57B6 mice and 2 knockout mouse strains lacking the function of the Tlr4 and Myd88 genes on embryonic day 15. Intrauterine injections of Escherichia coli lipopolysaccharide or saline were administered as described previously. Dams were killed 6 hours postsurgery, and placental, amniotic fluid, and fetal brain tissue were collected. To assess brain injury, quantitative polymerase chain reaction (qPCR) analysis was performed on multiple components of the NOTCH signaling pathway, including Hes genes. Interleukin (IL) IL6, IL1β, and CCL5 expression was assessed using qPCR and enzyme-linked immunosorbent assay. Results: Using an established mouse model of intrauterine inflammation, we demonstrate that the abrogation of TLR4 signaling eliminates the cytokine response in mother and fetus and prevents brain injury associated with increased expression of transcriptional effectors of the NOTCH signaling pathway, Hes1 and Hes5. Conclusions: These data show that the activation of the TLR4 signaling pathway is necessary for the development of fetal brain injury in response to intrauterine inflammation.

Icariside II potentiates paclitaxel-induced apoptosis in human melanoma A375 cells by inhibiting TLR4 signaling pathway

2012 ◽  
Vol 50 (9) ◽  
pp. 3019-3024 ◽  
Author(s):  
Jinfeng Wu ◽  
Ming Guan ◽  
Pok Fai Wong ◽  
Howard Yu ◽  
Jingcheng Dong ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Human Melanoma ◽  
Tlr4 Signaling ◽  
Icariside Ii ◽  
Tlr4 Signaling Pathway ◽  
Induced Apoptosis ◽  
A375 Cells
Sign in / Sign up

Export Citation Format

Share Document