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           Search results for: Human Tumor Necrosis Factor alpha TNF-α   

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#28934245   2017/09/21 Save this To Up

Angiopoietin-like protein 2 regulates Porphyromonas gingivalis lipopolysaccharide-induced inflammatory response in human gingival epithelial cells.

Angiopoietin-like protein 2 (ANGPTL2) maintains tissue homeostasis by inducing inflammation and angiogenesis. It is produced in infiltrating immune cells or resident cells, such as adipocytes, vascular endothelial cells, and tumor cells. We hypothesized that ANGPTL2 might play an important role as a unique mediator in both systemic and periodontal disease. We demonstrated an increased ANGPTL2 concentration in gingival crevicular fluid from chronic periodontitis patients. Porphyromonas gingivalis lipopolysaccharide (LPS) treatment strongly induced ANGPTL2 mRNA and protein levels in Ca9-22 human gingival epithelial cells. Recombinant human ANGPTL2 increased interleukin 1β (IL-1β), IL-8, and tumor necrosis factor-α (TNF-α) mRNA and protein levels in Ca9-22 cells. Small-interfering (si)RNA-mediated ANGPTL2 knockdown in Ca9-22 cells reduced IL-1β, IL-8 and TNF-α mRNA and protein levels compared with control siRNA (p<0.01) in P. gingivalis LPS-stimulated Ca9-22 cells. Antibodies against integrin α5β1, an ANGPTL receptor, blocked induction of these inflammatory cytokines in P. gingivalis LPS-treated Ca9-22 cells, suggesting that secreted ANGPTL induces inflammatory cytokines in gingival epithelial cells via an autocrine loop. The classic sequential cascade of P. gingivalis LPS → inflammatory cytokine induction is well established. However, in the current study, we reveal a novel cascade comprising sequential P. gingivalis LPS → ANGPTL2 → integrin α5β1 → inflammatory cytokine induction, which might be responsible for inducing potent periodontal disorganization activity in gingival epithelial cells. Via this pathway, ANGPTL2 functions in the pathogenesis of periodontitis and contributes to prolonging chronic inflammation in patients with systemic disease.

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#28933476   2017/09/21 Save this To Up

Piceatannol inhibits the IL-1β-induced inflammatory response in human osteoarthritic chondrocytes and ameliorates osteoarthritis in mice by activating Nrf2.

Osteoarthritis (OA) is a complex process, to which an inflammatory environment contributes markedly. Piceatannol exerts anti-inflammatory effects on several diseases. In the current study, we explored the protective effects of piceatannol on the progression of OA and investigated its molecular target. In vitro, piceatannol not only attenuated the over-production of inflammatory mediators and cytokines-such as nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6)-but also suppressed the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) at both the mRNA and protein levels. Piceatannol also decreased the expression of metalloproteinase 13 (MMP13) and thrombospondin motifs 5 (ADAMTS5), which mediate extracellular matrix degradation. Mechanistically, we found that piceatannol inhibited IL-1β-induced nuclear factor kappa B (NF-κB) activation by activating the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway. Furthermore, piceatannol exerted protective effects in a mouse model of OA. Taken together, these findings indicate that piceatannol may be a potential therapeutic agent for OA.

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#28930874   2017/09/20 Save this To Up

The Effectiveness of Fish Oil Supplementation in Attenuating Exercise-Induced Muscle Damage in Females During Mid-Follicular and Mid-Luteal Menstrual Phases.

The purpose of this study was to determine if the differences in estrogen levels during the female menstrual cycle and fish oil supplementation would attenuate eccentric exercise-induced muscle damage (EIMD) and delayed onset muscle soreness (DOMS). In a double-blind fashion, 22 physically-active females (20.9 ± 1.4 years, 63.5 ± 9.0 kg, 165.2 ± 7.5 cm) were randomly assigned to ingest either 6 grams of fish oil (n = 11) or placebo (n = 11) daily for 21 days. Participants underwent an eccentric exercise bout of the knee extensors on two occasions during the mid-follicular (MF) and mid-luteal (ML) phases of the 28-day menstrual cycle. Prior to (PRE), at 6 (6HRPOST), and 24 hours post-exercise (24HRPOST) for each session, participants underwent assessments of DOMS, muscle strength, and had venous blood samples and muscle biopsies obtained. Data were analyzed utilizing a 2 x 2 x 3 repeated measures multivariate analyses of variance for each criterion variable (p ≤ .05). Further analysis of the main effects for Test was performed by separate one-way analyses of variance. DOMS was significantly greater at the 6HRPOST and 24HRPOST time points compared to PRE (p < .001). Superoxide dismutase and tumor necrosis factor-alpha (TNF-α) concentrations were significantly higher at the MF phase compared to the ML phase (p < .001 and p = .05, respectively). There were no statistically significant differences observed for muscle strength, myoglobin, NF-Kβ p50 or NF-Kβ p65. This study demonstrates that higher levels of estrogen may exert a cyto-protective effect on the sarcolemma.

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#28928738   2017/09/20 Save this To Up

Age-Stratified T Cell Responses in Children Infected with Mycobacterium tuberculosis.

Tuberculosis (TB) in young children differs from adult TB in that the risk of rapid progression to active TB (aTB) is higher in children than in adults. The reasons for this increased risk are not fully understood. Early differentiation remains difficult between children at risk to develop aTB from those who will remain healthy and develop a latent TB infection (LTBI). Biomarkers to differentiate aTB from LTBI in children, especially in very young children, are urgently needed. To identify M. tuberculosis-specific functional T cell subsets related to clinical manifestations in children, we enrolled 87 children exposed to M. tuberculosis. After standard clinical assessment, the children were classified as aTB, LTBI, or uninfected. Their CD4(+) T cell cytokine profiles (IFN-γ, TNF-α, IL-2, IL-17) were analyzed at the single-cell level by flow cytometry after stimulation with three mycobacterial antigens, purified protein derivative (PPD), early-secreted-antigenic target-6 (ESAT-6), or heparin-binding hemagglutinin (HBHA). This approach identified age-related discriminative markers between aTB and LTBI. Whereas among the 3- to 15-year-old children, an excellent discrimination between aTB and LTBI was provided by comparing the ratio between the proportions of ESAT-6-induced IFN-γ(single+) and ESAT-6-induced TNF-α(single+)CD4(+) T lymphocytes, this was not the case for children younger than 3 years. By contrast, in this group (<3years), the analysis of HBHA-induced IL-17(single+)CD4(+) T lymphocytes allowed us to identify children with LTBI by the high proportion of this cellular lymphocyte subset, whereas this was not the case for children with aTB. The analysis at the single-cell level of T cell immune responses induced by mycobacterial antigens are, thus, different in infected children younger or older than 3 years of age. HBHA-induced IL-17 production by CD4(+) T lymphocytes was associated with protection only in children under 3 years who are at high risk for rapid progression to aTB. This suggests that the HBHA-induced IL-17 production by CD4(+) T lymphocytes is a potential new correlate of protection against M. tuberculosis in humans, and that the distinction between children with LTBI and those with aTB is possible based on age-related diagnostic markers.

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#28928366   2017/09/20 Save this To Up

Fibromyalgia and microglial TNF-α: Translational research using human blood induced microglia-like cells.

Fibromyalgia is a refractory disease characterized by chronic intractable pain and psychological suffering, the cause of which has not yet been elucidated due to its complex pathology. Activation of immune cells in the brain called microglia has attracted attention as a potential underlying pathological mechanism in chronic pain. Until recently, however, technological and ethical considerations have limited the ability to conduct research using human microglia. To overcome this limitation, we have recently developed a technique to create human-induced microglia-like (iMG) cells from human peripheral blood monocytes. In this study, we created the iMG cells from 14 patients with fibromyalgia and 10 healthy individuals, and compared the activation of iMG cells between two groups at the cellular level. The expression of tumor necrosis factor (TNF)-α at mRNA and protein levels significantly increased in ATP-stimulated iMG cells from patients with fibromyalgia compared to cells from healthy individuals. Interestingly, there was a moderate correlation between ATP-induced upregulation of TNF-α expression and clinical parameters of subjective pain and other mental manifestations of fibromyalgia. These findings suggest that microglia in patients with fibromyalgia are hypersensitive to ATP. TNF-α from microglia may be a key factor underlying the complex pathology of fibromyalgia.

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#28927419   2017/09/20 Save this To Up

Tumor necrosis factor superfamily ligand mRNA expression profiles differ between humans and mice during homeostasis and between various murine kidney injuries.

Several tumour necrosis factor (TNF) based therapeutics have already been approved for human use and several others are emerging. Therefore, we determined the mRNA expression levels of the TNF superfamily ligands (TNFSF) - e.g. TNF-α, lymphotoxin (LT)-α, LT-β, Fas-L (CD95-L), TNF-related apoptosis-inducing ligand (TRAIL), TNF-related weak inducer of apoptosis (TWEAK), 4-1BBL, OX40-L (CD252) and amyloid precursor protein (APP) in healthy human and mouse solid organs.

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#28926879   2017/09/19 Save this To Up

[Systematic evaluation on effectiveness and safety of recombinant human growth hormone in treating adult patients with severe burn].

Objective: To systcmatically evaluate the effectiveness and safety of recombinant human growth hormone (rhGH) in treating adults with severe burn. Methods: Databases including PubMed, Cochrane Library, and Embase were searched using key words " burns, thermal, human growth hormone, growth hormone, hGH, and somatropin (human)" , and China Biology Medicine disc, Chinese Journals Full-text Database, VIP Database, and Wanfang Database were searched using key words in Chinese version "," to obtain the randomized controlled trials about rhGH in the treatment of adults with severe burn from the establishment of each database to December 2016. The measurement indexes included hemoglobin (Hb) and plasma total protein, inflammatory factors [including interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α)], incidence rate of sepsis, incidence rate of hyperglycemia, wound healing time, length of stay, and mortality rate. Meta-analysis was conducted by RevMan 5.3 statistical software. Results: A total of 8 trials involving 534 patients were included; 276 patients in rhGH group were treated with rhGH and 258 patients in placebo control group were treated with placebo. One trial had low risk of bias, while the other 7 trials had unclear risk of bias. The levels of Hb and plasma total protein of patients in rhGH group were higher than those in placebo control group, with standardized mean differences (SMDs) respectively 2.00 and 2.23 [with 95% confidence intervals (CIs) respectively 0.19-3.82 and 1.21-3.26, P<0.05 or P<0.01]. The levels of IL-6 and TNF-α of patients in rhGH group were lower than those in placebo control group, with SMDs respectively -1.46 and -1.13 (with 95% CIs respectively -2.40--0.53 and -1.75--0.51, P values below 0.05). Incidence rate of sepsis and mortality rate of patients in rhGH group were lower than those in placebo control group, with relative risks (RRs) respectively 0.60 and 0.35 (with 95% CIs respectively 0.42-0.85 and 0.15-0.83, P values below 0.05). Incidence rate of hyperglycemia of patients in rhGH group was higher than that in placebo control group, with RR of 2.39 (with 95% CI 1.79-3.18, P<0.001). The wound healing time and length of stay of patients in rhGH group were lower than those in control group, with SMDs respectively -1.54 and -2.00 (with 95% CIs respectively -2.22--0.86 and -3.51--0.49, P<0.05 or P<0.01). Hb, plasma total protein, inflammatory factors, incidence rate of sepsis, wound healing time, length of stay, and mortality rate showed no significant publication bias (P values above 0.05), while there may be publication bias in incidence rate of hyperglycemia (P=0.026). Conclusions: rhGH can inhibit the breakdown of Hb and plasma total protein, reduce the level of inflammatory factors and incidence rate of sepsis, thus shorten the wound healing time and length of stay, thereby reduce mortality rate of adult patients with severe burn. However rhGH may cause hyperglycemia.

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#28925826   2017/09/19 Save this To Up

Tumor necrosis factor-α inhibits chondrogenic differentiation of synovial fibroblasts through p38 mitogen activating protein kinase pathways.

We previously reported that synovial fibroblast-like cells (SFs) can be differentiated into chondrocytes through activin receptor-like kinase (ALK) 3 activation. The aim of this study was to clarify the effect and signaling pathways of tumor necrosis factor (TNF)-α on the chondrogenic differentiation of SFs. Primary SFs from patients with rheumatoid arthritis (RA) were treated with recombinant human bone morphogenetic protein-2 or transduced with a constitutively active mutant of the ALK3 gene (ALK3(CA)) with or without TNF-α, and then cultured in pellets. Expression of chondrocyte-specific genes was analyzed by real-time polymerase chain reaction or by histological analysis. Inhibitors of mitogen-activating protein kinase (MAPK) pathways or adenovirus vectors carrying a dominant-negative mutant of the IκB kinase 2 gene (AxIKK2(DN)) were used to analyze the signaling pathways of TNF-α. Expression of chondrocyte-specific genes was induced in SFs either by rhBMP-2 treatment or by ALK3(CA) transduction, which was strongly suppressed by TNF-α treatment. TNF-α markedly increased the p38 MAPK pathways in SFs, and inhibition of p38 MAPK activation partially restored the inhibitory effect of TNF-α on the chondrogenic differentiation of SFs. Combination therapy BMP-2 and anti-TNF-α agents especially targeting p38 MAPK might be a good approach to stimulating neochondrogenesis in the damaged joints in RA.

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#28925311   2017/09/19 Save this To Up

Combining effects of polymorphism of tumor necrosis factor α 5'-flanking region and HLA-DRB1 on radiological progression in patients with rheumatoid arthritis.

We examined whether polymorphisms upstream of the TNF-α gene (TNFA) were associated with the radiological progression of rheumatoid arthritis (RA). One hundred and twenty-three patients with early RA (disease duration <1 year) were enrolled in a prospective follow-up study. The laboratory findings (ESR, CRP, and RF) were evaluated every 2 months for 2 years. Radiological progression in hands/wrists and feet was evaluated every 6 months for 2 years using Larsen's score. HLA-DRB1 genotype was determined by PCR-RFLP method. The genotypes for -1031, -863, and -857 single-nucleotide polymorphisms in the upstream 5'-flanking region of TNFA were determined by a PCR-preferential homoduplex formation assay in patients with RA and 265 healthy controls. Four TNFA alleles (U01, U02, U03, and U04) were identified. The frequency of individuals with U02 was significantly higher in patients than in controls (P = 0.0025). Radiographs of hands/wrists/feet were available for 72 patients after 1 year and for 73 patients after 2 years. When the HLA-DRB1 genotype was analyzed simultaneously, patients possessing U02 without an HLA-DRB1 shared epitope (SE) (U02+SE-) showed the lowest progression of Larsen's score (12 months). There was no difference in the level of ESR, CRP, or RF at the first visit among U02+SE+, U02+SE-, U02-SE+, and U02-SE- groups. The combination of the polymorphism of the TNFA upstream promoter region and HLA-DRB1 allele was associated with radiological progression in the early stage of RA.

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#28922714   2017/09/19 Save this To Up

Atmospheric levels and cytotoxicity of polycyclic aromatic hydrocarbons and oxygenated-PAHs in PM2.5 in the Beijing-Tianjin-Hebei region.

The chemical composition of PM2.5 and cellular effects from exposure to fine aerosol extracts were studied for samples collected in Beijing, Tianjin, Shijiazhuang, and Hengshui, China in winter 2015. Effects of priority polycyclic aromatic hydrocarbons (PAHs) and their oxygenated derivatives (OPAHs) in PM2.5 on cell cultures were a major focus of the study. Total quantified PAHs and OPAHs at Shijiazhuang and Hengshui were higher than at Beijing and Tianjin, and benz(a)anthracene, chrysene and 1,8-naphthalic anhydride were the most abundant species. Exposure to PM2.5 extracts caused a concentration-dependent decline in cell viability and a dose-dependent increase in nitric oxide production. Two cytokines, tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), also increased when A549 test cells were exposed to PM2.5 extracts. PAHs and OPAHs in PM2.5 can potentially cause cell damage and induce cytotoxicity and pro-inflammatory responses: benzo(a)anthracene-7,12-dione was highly correlated with NO production, dibenz(a,h)anthracene and 1,4-chrysenequinone were correlated with TNF-α production, and 1-naphthaldehyde was significantly correlated with IL-6 production. The study provides a new approach for evaluating relationships between air-quality and cell toxicity with respect to specific chemicals.

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