scholarly journals Protective Role of Toll-like Receptor 4 during the Initiation Stage of Cutaneous Chemical Carcinogenesis

2008 ◽  
Vol 68 (2) ◽  
pp. 615-622 ◽  
Author(s):  
Nabiha Yusuf ◽  
Tahseen H. Nasti ◽  
J. Alan Long ◽  
Mohammed Naseemuddin ◽  
Alan P. Lucas ◽  
...  
Keyword(s):  
Chemical Carcinogenesis ◽  
Protective Role ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Initiation Stage

scholarly journals Protective role of Toll-like receptor 4 in experimental gonococcal infection of female mice

2011 ◽  
Vol 5 (1) ◽  
pp. 19-29 ◽  
Author(s):  
M Packiam ◽  
H Wu ◽  
S J Veit ◽  
N Mavrogiorgos ◽  
A E Jerse ◽  
...  
Keyword(s):  
Protective Role ◽  
Toll Like Receptor ◽  
Gonococcal Infection ◽  
Toll Like Receptor 4 ◽  
Female Mice

scholarly journals Astragaloside IV alleviates placental oxidative stress and inflammation in GDM mice

2020 ◽  
Vol 9 (9) ◽  
pp. 939-945
Author(s):  
Ling Zhou ◽  
Ruixue Zhang ◽  
Shuangyan Yang ◽  
Yaguang Zhang ◽  
Dandan Shi
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Protective Role ◽  
The Other ◽  
Toll Like Receptor ◽  
Astragaloside Iv ◽  
Toll Like Receptor 4 ◽  
Pregnant Mice ◽  
Placental Oxidative Stress

Background: Our previous study revealed that astragaloside IV (AS-IV) effectively improved gestational diabetes mellitus (GDM) by reducing hepatic gluconeogenesis. Due to the importance of placental oxidative stress, we further explored the protective role of AS-IV on placental oxidative stress in GDM. Methods: First, non-pregnant mice were orally administrated with AS-IV to evaluate its safety and effect. Then GDM mice were orally administered with AS-IV for 20 days and its effect on the symptoms of GDM, placental oxidative stress, secretions of inflammatory cytokines, as well as toll-like receptor 4 (TLR4)/NF-κB signaling pathway, were evaluated. Results: AS-IV had no adverse effect on non-pregnant mice. On the other hand, AS-IV significantly attenuated the GDM-induced hyperglycemia, glucose intolerance, insulin resistance, placental oxidative stress, productions of inflammatory cytokines and the activation of TLR4/NF-κB pathway. Conclusion: AS-IV effectively protected against GDM by alleviating placental oxidative stress and inflammation, in which TLR4/NF-κB might be involved.

Evaluation of toll-like receptor 4 polymorphism in patients with hepatitis c virus-induced hepatocellular carcinoma

2021 ◽  
Vol 30 (3) ◽  
pp. 1-8
Author(s):  
Fatma O. Khalil ◽  
Mohammed A. Rady ◽  
Seham A. Eissa ◽  
Azza M. Abd El Aziz
Keyword(s):  
Hepatocellular Carcinoma ◽  
Protective Role ◽  
Control Group ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Development Methodology ◽  
Pathogen Recognition Receptors ◽  
Chronic Hcv ◽  
Tlr4 Receptor

Background: Liver related pathologies including Hepatocellular Carcinoma (HCC) is a universal problem. Innate immunity receptors were accused in the etiopathogenesis of HCC with many conflicts. TLR4 is one of pathogen recognition receptors involved in the pathogenesis of many diseases and malignancies. TLR4 receptor polymorphisms were investigated in HCV related morbidities along with inconclusive results Objectives: to study the role of TLR4 rs 2149356 and rs 1927914 genotypes polymorphisms in HCV related HCC development. Methodology: 200 Chronically infected HCV patients were enrolled in this study. they were divided according to lab and clinical data into 100 CHC group and 100 HCC patients who were compared to health individual. The blood samples obtained were further proceed to full lab and TLR4 genotyping by RFLP-PCR technique Results: GT genotype and T allele of TLR4 rs 2149356 at 95% CI of 0.38 (0.21-0.70) was significantly increased in control group than in HCC and CHC groups. At 0.32(0.17-0.63) TLR4 rs 1927914 C allele and CT genotype was significantly increased in Controls than diseased groups while T allele is significantly increased in HCC than control group. Conclusions: TLR4 genotypes may play a protective role against HCC development among chronic HCV patients.

The Protective Role of Host Toll-Like Receptor-4 in Acute Graft-Versus-Host Disease

2010 ◽  
Vol 90 (10) ◽  
pp. 1063-1070 ◽  
Author(s):  
Takehito Imado ◽  
Tsuyoshi Iwasaki ◽  
Sachie Kitano ◽  
Atsushi Satake ◽  
Takanori Kuroiwa ◽  
...  
Keyword(s):  
Graft Versus Host Disease ◽  
Protective Role ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Host Disease ◽  
Graft Versus Host ◽  
Acute Graft

scholarly journals Detrimental Role of Heat Shock Protein 60&70 and Toll-like Receptor 4 in Skeletal Muscle Ischaemia In Vitro

2013 ◽  
Vol 57 (5) ◽  
pp. 77S
Author(s):  
Ali Navi ◽  
Rebekah Yu ◽  
Xu Shi-Wen ◽  
Sidney Shaw ◽  
George Hamilton ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 60 ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Muscle Ischaemia

Contrasting effects of the Toll-like receptor 4 in determining ovarian follicle endowment and fertility in female adult mice

Zygote ◽  
2021 ◽  
pp. 1-7
Author(s):  
Júlio Panzera Gonçalves ◽  
Breno Augusto Magalhães ◽  
Paulo Henrique Almeida Campos-Junior
Keyword(s):  
Ovarian Follicle ◽  
Cumulus Cells ◽  
Toll Like Receptor ◽  
Female Reproduction ◽  
Toll Like Receptor 4 ◽  
Genetic Ablation ◽  
Adult Mice ◽  
Cumulus Oocyte Complex ◽  
Estrous Cyclicity

Abstract Toll-like receptor 4 (TLR4) is best known for its role in bacteria-produced lipopolysaccharide recognition. Regarding female reproduction, TLR4 is expressed by murine cumulus cells and participates in ovulation and in cumulus–oocyte complex (COC) expansion, maternal–fetal interaction and preterm labour. Despite these facts, the role of TLR4 in ovarian physiology is not fully understood. Therefore, the aim of the present study was to investigate the effects of TLR4 genetic ablation on mice folliculogenesis and female fertility, through analysis of reproductive crosses, ovarian responsiveness and follicular quantification in TLR4−/− (n = 94) and C57BL/6 mice [wild type (WT), n = 102]. TLR4-deficient pairs showed a reduced number of pups per litter (P = 0.037) compared with WT. TLR4−/− mice presented more primordial, primary, secondary and antral follicles (P < 0.001), however there was no difference in estrous cyclicity (P > 0.05). A lower (P = 0.006) number of COC was recovered from TLR4−/− mice oviducts after superovulation, and in heterozygous pairs, TLR4−/− females also showed a reduction in the pregnancy rate and in the number of fetuses per uterus (P = 0.007) when compared with WT. Altogether, these data suggest that TLR4 plays a role in the regulation of murine folliculogenesis and in determining ovarian endowment. TLR4 deficiency may affect ovulation and pregnancy rates, potentially decreasing fertility, therefore the potential side effects of its blockade have to be carefully investigated.

Abstract 1766: Diet-Induced Obesity Causes Inflammation by Activating Toll-Like Receptor 4 Signaling and Downregulates AMPK in Heart

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Hwi Jin Ko ◽  
Dae Young Jung ◽  
Zhexi Ma ◽  
Jason K Kim
Keyword(s):  
Glucose Metabolism ◽  
Whole Body ◽  
Chow Diet ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Myocardial Glucose Metabolism ◽  
Cardiac Inflammation ◽  
Protein Levels ◽  
Diet Induced Obesity

Increasing evidence implicates the role of inflammation in diabetes and complications. Macrophages are shown to infiltrate adipose tissue in obesity, and inflammatory cytokines alter glucose metabolism in peripheral organs. Male C57BL/6 mice were fed high-fat diet (HFD; 55% fat by calories) or chow diet for 6 weeks, and heart samples were taken for analysis (n = 5~7). Chronic HFD increased whole body fat mass, measured by 1 H-MRS, by 3-fold, and elevated plasma IL-6 and TNF-α levels by 40%. Diet-induced obesity caused inflammation in heart and increased macrophage-specific CD68 levels by 5-fold (Fig. 1) (* P < 0.05 vs Chow). Diet-induced cardiac inflammation was associated with significant increases in toll-like receptor 4 (TLR4) and MyD88 levels in heart (Fig. 2). HFD also increased cardiomyocyte SOCS3 levels by more than 3-fold (Fig. 3). Myocardial glucose metabolism was measured using intravenous injection of 2-[ 14 C]deoxyglucose in awake mice (n = 6). Chronic HFD reduced myocardial glucose uptake by 50%, and this was associated with significant reductions in total GLUT4 and GLUT1 protein levels. Further, Thr 172 phosphorylation of AMPK, a critical regulator of energy balance, was markedly reduced in heart following HFD (Fig. 4). These results demonstrate that diet-induced obesity causes macrophage infiltration and inflammation in heart by increasing TLR4 signaling in cardiomyocytes. Similar to the effects of inflammation on peripheral glucose metabolism, diet-induced cardiac inflammation reduced myocardial glucose metabolism by downregulating AMPK and GLUT protein levels. Thus, our findings underscore an important role of inflammation in diabetic heart.

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