Search results for: Cytokine
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Catalpol ameliorates Sjögren's Syndrome by modulating interplay of T and B cells.Catalpol is an active ingredient of Rehmanniae Radix, a medical herb used frequently in treating primary Sjogren's Syndrome (pSS). However, no study has assessed the therapeutic effects of catalpol in treating Sjogren's Syndrome. This study aimed to investigate the therapeutic effects of catalpol for pSS by evaluating the water consumption, stimulated salivary flow rates, sialadenitis, T cell subsets and related cytokine levels. Catalpol treated mice had improved stimulated salivary flow rates and water consumption compared to mice from the control group. Catalpol also reduced the lymphocytic infiltration and prevented the formation of ectopic germinal centers. These effects, especially in the catalpol high dose group, were associated with elevated CD4 CXC-R5 PD-1 Foxp3 T follicular regulatory (Tfr) cells (1.572 % vs 1.118 %, P = 0.0005) and a higher ratio of Tfr cells to T follicular helper (Tfh) cells (2.137 vs 1.541, P = 0.0007). Downregulated levels of IFN-γ and BAFF in serum and submandibular glands were also noted in catalpol treated groups. Our work indicated that catalpol might be a potential drug for treating pSS by regulating the interplay between T and B cells.
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Casticin elicits inflammasome-induced pyroptosis through activating PKR/JNK/NF-κB signal in 5-8F cells.Casticin is one of the effective ingredients of fructus viticis. Most studies have shown that casticin has a strong anti-proliferation activity against various tumor cells. However, its anti-tumor effect and molecular mechanism in nasopharyngeal carcinoma remain unclear. In this study, we demonstrated that the casticin selectively inhibited the proliferation of 5-8F cells in vitro. Further analysis revealed that casticin treatment significantly increased sub-G2 phase and incited pyroptotic process. Moreover, we demonstrated that PKR participated in in regulating the process of GSDMD-dependent pyroptotic tumor cell death. PKR knockdown alleviated the activation of JNK pathway and the expression of its downstream proteins, including cleaved caspase-1, GSDMD-N, interleukin-1β. These findings indicate that PKR/JNK/NF-κB signal is essential for casticin-induced caspase-1 inflammasome formation and inflammatory cytokines release in 5-8F cell.
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Interleukin-17 mRNA expression and serum levels in Behçet's disease.Behçet's disease (BD) was considered a T-helper 1 (Th1)-mediated autoimmune disease, but with the introduction of Th17 cells, their role in the pathogenesis of BD was also addressed. Despite studies on IL-17 in BD, the prognostic value of this cytokine in BD is unclear. The aim of this study is to determine the IL-17 mRNA expression rate and serum levels in patients with BD and its correlation with clinical manifestations and activity of BD. Forty-six BD patients in the active phase of the disease and 70 healthy controls were recruited in this study. BD activity was measured by Behçet's disease current activity form (BDCAF), Iranian Behçet's disease dynamic activity measure (IBDDAM) and total inflammatory activity index (TIAI). The IL-17 mRNA expression and serum levels were significantly higher in the BD patients compared with the healthy controls. These parameters in the BD patients aged <25 at disease onset, positive pathergy test, and positive HLA-B5 and HA-B51 were significantly higher than the healthy controls (P < 0.05). The IL-17 serum level in the patients with active uveitis was lower than the patients with in-active uveitis. There was no association between other clinical manifestations of BD and these parameters. No significant correlation was found between BDCAF and IBDDAM with IL-17 mRNA expression and serum levels. However, TIAI had a significant and negative correlation with the serum levels of IL-17.
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Hypoxia upregulates Cxcl12 in hepatocytes by a complex mechanism involving hypoxia-inducible factors and transforming growth factor-β.Cxcl12, or stromal-derived factor-1, is a chemokine produced by several hepatic cell types, including hepatocytes, after liver injury and surgical resection. Studies have revealed that Cxcl12 is important for regeneration of the liver after surgical resection and for development of liver fibrosis during chronic liver injury. While the function of Cxcl12 in the liver is well established, the mechanism by which Cxcl12 is upregulated is not fully understood. Because regions of hypoxia develop in the liver following injury, we tested the hypothesis that hypoxia upregulates Cxcl12 in hepatocytes by a hypoxia-inducible factor (HIF)-dependent mechanism.
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Promoter polymorphisms in IL-6 gene influence pro-inflammatory cytokines for the risk of osteoarthritis.Interleukin-6 (IL-6) gene regulates IL-6 levels, interplay of which has been found to influence pathophysiology of osteoarthritis (OA). Polymorphism within promoter region of IL-6 gene and its association with plasma levels of pro-inflammatory cytokines; IL-6, interleukin 1-beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) remained to be investigated in Punjab region of India, where OA is highly prevalent.
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Effects of maternal and fetal vascular endothelial growth factor a single nucleotide polymorphisms on pre-eclampsia: A hybrid design study.Maternal and fetal gene variants play important roles in the pathology of pre-eclampsia (PE), but most studies investigating the associations between vascular endothelial growth factor A (VEGF-A) gene variates and PE focusing on maternal genetic effects. The present study firstly used a hybrid case-parent and control-mother study design investigating the both maternal and fetal effects of VEGF-A gene polymorphisms on PE among Han Chinese pregnant women. This study recruited 221 PE patients with their partners and infants and 345 normotensive women with their infants. The current study found that, in both maternal and fetal dominant model (GC + CC/GG), VEGF-A rs2010963 polymorphism was associated with an increased risk of PE (OR = 1.85, 95% CI: 1.25-2.75; OR = 1.90, 95% CI: 1.28-2.83, respectively). In the log-liner model analyses, offspring carrying the genotype of GC or CC in the rs2010963 polymorphism could increase the risk of maternal PE (OR = 1.84, 95%CI: 1.18-2.86; OR = 1.89, 95%CI: 1.02-3.49, respectively) compared to the offspring with GG. Meanwhile, the present study also found that passive smoking had a significant interaction with maternal rs2010963 polymorphism (P = 0.022) on the risk of PE.
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Dysregulation of renal transporters in a rodent model of viral Infection.Inflammation elicited by viral mimetic poly I:C has been shown to impose changes in the expression of drug transporters in the placenta and maternal liver in rats at term pregnancy. This was associated with altered drug disposition in the mother and fetus. Renal transporters play an important role in the elimination of several drugs taken by pregnant women. We examined the impact of poly I:C on the expression of renal transporters in pregnant rats at term. Pregnant Sprague-Dawley rats received single intraperitoneal dose of either poly I:C (5 mg/kg) or saline at gestation day 18 (n = 8/group). Animals were euthanized 24 h after the injection. The mRNA and protein expression of pro-inflammatory cytokines and transporters were measured by qRT-PCR and western blot. Poly I:C caused a fourfold increase in the mRNA of IL-6 in the kidney. As compared to saline controls, the mRNA expression of Mrp2, Bcrp, Octn1, Oat1, Oat2, Oat3, Urat1, Oatp4c1, and Pept2 was downregulated, whereas the Ent1 mRNA was increased. Protein expression of Bcrp, Urat1 and Pept2 were significantly decreased. While there was a trend towards reduced Mrp2, Oat2 and Oat3 protein expression, this did not reach significance. Poly I:C did not impact mRNA levels of Mdr1a, Mdr1b, Mrp4, Oct1, Oct2, Oct3, Octn2, Mate1, Ent2 or Pept1. Viral-induced inflammation mediates significant changes in the expression of several key drug transporters in the kidney of pregnant rats. Many clinically important drugs are substrates for these transporters. Therefore, inflammation-mediated alterations in transporter expression could affect their maternal and fetal disposition.
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Attenuation of paraquat-induced inflammation by inhibitors of phosphorylation of mitogen-activated protein kinases in BV microglial cells.Paraquat has dopaminergic neurotoxicity and potentially contributes to Parkinson's disease (PD) as a risk factor. However, the cellular and molecular mechanisms of PQ-induced neurodegeneration have not been clearly elucidated. Studies have shown that PQ induces microglial neuroinflammation through toll-like receptor 4 (TLR4)-nuclear factor-κB pathway, resulting in neuronal cell loss. Mitogen-activated protein kinases (MAPKs) are involved in the production of pro-inflammatory cytokines in microglia, and in this study, the role of MAPKs in PQ-activated microglial inflammation was investigated. Murine BV microglial cells were treated with 40 μM of PQ following pretreatment of the cells with selective inhibitor of MAPKs phosphorylation for blockage of the phosphorylation of ERK, JNK and P38, or a specific TLR4 inhibitor for blocking the activation of TLR4. The protein expression of phosphorylated ERK, JNK and p38, and the transcription expression of pro-inflammatory mediators were assessed with Western blotting and qRT-PCR technique, respectively. The results indicated that PQ significantly induced the phosphorylation of ERK, JNK and P38 in microglia, while MAPKs inhibitors suppressed PQ-induced phosphorylation of ERK, JNK and P38, and reduced the transcription level of pro-inflammatory cytokines. PQ-stimulated phosphorylation of ERK, JNK and P38 was also reduced by TLR4 inhibitor. The inhibited intensity in the level of pro-inflammatory cytokine transcription was obviously greater in TLR4 inhibitor + PQ group than in each MAPK inhibitor + PQ group. Taken together, inhibition of MAPKs phosphorylation partially attenuates PQ-induced microglial inflammation, which may become a potential intervention strategy for PQ neurotoxicity.
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Tryptophan metabolite-regulated Treg responses contribute to attenuation of airway inflammation during specific immunotherapy in a mouse asthma model.In allergen-specific immunotherapy for asthma, antigens attached to dendritic cells increase the tryptophan metabolism in these cells and alter the Th17/Treg balance in the airways. Tryptophan metabolism has long been suggested to be relevant in the pathophysiology of allergic disorders, including asthma. Our study investigated whether tryptophan metabolites are responsible for the changes in Th17/Treg balance and decreases in airway hyperreactivity and inflammation seen during allergen-specific immunotherapy in an asthma model. Ovalbumin was injected intraperitoneally into mice to establish an asthma model, and then high dose ovalbumin allergen-specific immunotherapy was administered to induce immune tolerance. Airway hyperreactivity and serum ovalbumin-specific immunoglobulin E were measured to assess whether the animal model was successfully established. We then examined the influence of inhibition of tryptophan metabolism and the addition of tryptophan metabolites on allergen-specific immunotherapy-induced changes in the Th17/Treg balance and decreases in airway inflammation and inflammatory cytokines. Production of tryptophan metabolites was partly responsible for the allergen-specific immunotherapy-induced increase in Tregs, decrease in airway inflammation, and decrease in inflammatory cytokines. Ovalbumin-specific immunoglobulin E and airway hyperreactivity were not affected. In the context of asthma, an increase in tryptophan metabolites is one of the mechanisms by which allergen-specific immunotherapy achieves immune tolerance.
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Integrated targeted serum metabolomic profile and its association with gender, age, disease severity, and pattern identification in acne.Westernized diet and nutritional metabolism are important in acne pathogenesis, especially in adult patients. However, clinical and basic data are lacking. Pattern identification (PI) is a tool that results in a diagnostic conclusion based on a cluster of concurrent symptoms and signs in traditional medicine. Acne can be classified by PI. However, whether the metabolomic profile differs according to the PI of acne is unknown. Metabolomic data would help clarify the pathogenesis of acne.
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