scholarly journals Toll-Like Receptor 4 Activation Reduces Adrenal Chromaffin Cell Excitability Through a Nuclear Factor-κB-Dependent Pathway

Endocrinology ◽  
2013 ◽  
Vol 154 (1) ◽  
pp. 351-362 ◽  
Author(s):  
Mark K. Lukewich ◽  
Alan E. Lomax
Keyword(s):  
Neuropeptide Y ◽  
Adrenal Medulla ◽  
Action Potentials ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Neuropeptide Y Release ◽  
Adrenal Chromaffin ◽  
Dependent Pathway

The adrenal medulla contains fenestrated capillaries that allow catecholamines and neuropeptides secreted by adrenal chromaffin cells (ACCs) to readily access the circulation. These capillaries may also allow bacterial products to enter the adrenal medulla and interact with ACCs during infection. One potential mediator of this interaction is toll-like receptor 4 (TLR-4), a pattern-recognition receptor that detects lipopolysaccharide (LPS) from Gram-negative bacteria. Evidence suggests that excitable cells can express TLR-4 and that LPS can modulate important neuronal and endocrine functions. The present study was therefore performed to test the hypothesis that TLR-4 activation by LPS affects ACC excitability and secretory output. RT-PCR revealed that TLR-4, cluster of differentiation 14, myeloid differentiation protein-2, and myeloid-derived factor 88 are expressed within mouse adrenal medullae. TLR-4 immunoreactivity was observed within all tyrosine hydroxylase immunoreactive ACCs. Incubation of isolated ACCs in LPS dose dependently hyperpolarized the resting membrane potential and enhanced large conductance (BK) Ca2+-activated K+ currents. LPS (10 μg/ml) also increased rheobase, decreased the number of action potentials fired at rheobase, and reduced the percentage of ACCs exhibiting spontaneous and anodal break action potentials. Although catecholamine release was unaltered, LPS significantly reduced high-K+-stimulated neuropeptide Y release from isolated ACCs. LPS did not alter the excitability of ACCs from TLR-4−/− mice. Inhibition of nuclear factor-κB signaling with SC-514 (20 μm) abolished the effects of LPS on ACC excitability. Our findings suggest that LPS acts at TLR-4 to reduce ACC excitability and neuropeptide Y release through an nuclear factor-κB-dependent pathway.

scholarly journals CD4+CD25+Foxp3+ regulatory T cells regulate immune balance in unexplained recurrent spontaneous abortion via the Toll-like receptor 4/nuclear factor-κB pathway

2020 ◽  
Vol 48 (12) ◽  
pp. 030006052098094
Author(s):  
Shuang Qin ◽  
Li Li ◽  
Jia Liu ◽  
Jinrui Zhang ◽  
Qing Xiao ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Inflammatory Response ◽  
Mouse Model ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Unexplained Recurrent Spontaneous Abortion ◽  
Tlr4 Antagonist

Objective The present study aimed to evaluate the effects of cluster of differentiation (CD)4+CD25+ forkhead box p3 (Foxp3)+ regulatory T cells (Tregs) on unexplained recurrent spontaneous abortion (URSA) and the associated mechanisms. Methods The proportion of CD4+CD25+Foxp3+ Tregs and inflammatory cytokine concentrations in the peripheral blood of women with URSA were measured by flow cytometry and enzyme-linked immunosorbent assay, respectively. CBA/JxDBA/2J mating was used to establish an abortion-prone mouse model and the model mice were treated with the Toll-like receptor 4 (TLR4) antagonist E5564 and the TLR4 agonist lipopolysaccharide. Results The proportion of CD4+CD25+Foxp3+ Tregs was decreased and the inflammatory response was increased in women with URSA. In the abortion-prone mouse model, E5564 significantly increased the proportion of CD4+CD25+Foxp3+ Tregs, decreased the inflammatory response, and increased Foxp3 mRNA and protein expression. Lipopolysaccharide had adverse effects on the abortion-prone model. Conclusions These data suggest that CD4+CD25+Foxp3+ Tregs regulate immune homeostasis in URSA via the TLR4/nuclear factor-κB pathway, and that the TLR4 antagonist E5564 may be a novel and potential drug for treating URSA.

scholarly journals Rhein inhibits lipopolysaccharide-induced intestinal injury during sepsis by blocking the toll-like receptor 4 nuclear factor-κB pathway

2015 ◽  
Vol 12 (3) ◽  
pp. 4415-4421 ◽  
Author(s):  
KE ZHANG ◽  
XIAN FA JIAO ◽  
JIN XIU LI ◽  
XIAO WEN WANG
Keyword(s):  
Nuclear Factor Κb ◽  
Intestinal Injury ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4

scholarly journals miR‑146b‑5p inhibits tumorigenesis and metastasis of gallbladder cancer by targeting Toll‑like receptor 4 via the nuclear factor‑κB pathway

2021 ◽  
Vol 45 (4) ◽  
Author(s):  
Bin Ouyang ◽  
Ningfeng Pan ◽  
Haifeng Zhang ◽  
Chuanming Xing ◽  
Wu Ji
Keyword(s):  
Gallbladder Cancer ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4

scholarly journals Attenuation of ventilation-induced diaphragm dysfunction through toll-like receptor 4 and nuclear factor-κB in a murine endotoxemia model

2018 ◽  
Vol 98 (9) ◽  
pp. 1170-1183 ◽  
Author(s):  
Li-Fu Li ◽  
Yung-Yang Liu ◽  
Ning-Hung Chen ◽  
Yen-Huey Chen ◽  
Chung-Chi Huang ◽  
...  
Keyword(s):  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Diaphragm Dysfunction ◽  
Endotoxemia Model

scholarly journals Ginseng (Panax ginseng Meyer) Oligopeptides Protect Against Binge Drinking-Induced Liver Damage through Inhibiting Oxidative Stress and Inflammation in Rats

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1665 ◽  
Author(s):  
Rui Liu ◽  
Qi-He Chen ◽  
Jin-Wei Ren ◽  
Bin Sun ◽  
Xia-Xia Cai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Liver Injury ◽  
Binge Drinking ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Oxidative Stress Markers ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Stress Markers

Panax ginseng C.A. Meyer (ginseng) is an edible and traditional medicinal herb, which is reported to have a wide range of biological activity and pharmaceutical properties. There were more studies on ginsenoside and polysaccharides, but fewer on ginseng oligopeptides (GOPs), which are small molecule oligopeptides extracted from ginseng. The present study was designed to investigate the effects and underlying mechanism of ginseng oligopeptide (GOPs) on binge drinking-induced alcohol damage in rats. Sprague Dawley rats were randomly assigned to six groups (n = 10), rats in normal control group and alcohol model group was administered distilled water; rats in four GOPs intervention groups (at a dose of 0.0625, 0.125, 0.25, 0.5 g/kg of body weight, respectively) were administered GOPs once a day for 30 days. Experiment rats were intragastrically administered ethanol at a one-time dose of 7 g/kg of body weight after 30 days. The liver injury was measured through traditional liver enzymes, inflammatory cytokines, expression of oxidative stress markers, and histopathological examination. We found that the GOPs treatment could significantly improve serum alanine aminotransferase and aspartate aminotransferase, plasma lipopolysaccharide, and inflammatory cytokine levels, as well as the oxidative stress markers that were altered by alcohol. Moreover, GOPs treatment inhibited the protein expression of toll-like receptor 4, and repressed the inhibitor kappa Bα and nuclear factor-κB p65 in the liver. These findings suggested that GOPs have a significant protective effect on binge drinking-induced liver injury, and the mechanism possibly mediated by the partial inhibition of lipopolysaccharide—toll-like receptor 4-nuclear factor-κB p65 signaling in the liver.

scholarly journals Lipopolysaccharide inhibition of glucose production through the Toll-like receptor-4, myeloid differentiation factor 88, and nuclear factor κb pathway

Hepatology ◽  
2009 ◽  
Vol 50 (2) ◽  
pp. 592-600 ◽  
Author(s):  
Carl F. Raetzsch ◽  
Natasha L. Brooks ◽  
J. McKee Alderman ◽  
Kelli S. Moore ◽  
Peter A. Hosick ◽  
...  
Keyword(s):  
Glucose Production ◽  
Nuclear Factor Κb ◽  
Myeloid Differentiation ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Differentiation Factor ◽  
Myeloid Differentiation Factor 88 ◽  
Myeloid Differentiation Factor
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