PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32399117-4 2020 The aim of this study was to determine the association between TNF polymorphisms and tuberculosis in the presence of biomass smoke, cigarettes, and alcohol in a Mexican population. Alcohols 148-155 tumor necrosis factor Homo sapiens 63-66 33390773-6 2021 Acute alcohol exposure-induced leukocyte infiltration and pro-inflammation factors, including cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6), were blocked by MLE in proportion to MLE concentration. Alcohols 6-13 tumor necrosis factor Homo sapiens 120-147 33390773-6 2021 Acute alcohol exposure-induced leukocyte infiltration and pro-inflammation factors, including cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6), were blocked by MLE in proportion to MLE concentration. Alcohols 6-13 tumor necrosis factor Homo sapiens 149-158 33680846-0 2020 Tumour Necrosis Factor in Neuroplasticity, Neurogenesis and Alcohol Use Disorder. Alcohols 60-67 tumor necrosis factor Homo sapiens 0-22 33680846-3 2020 Tumour necrosis factor (TNF) is a well characterised neuroimmune signal but its involvement in alcohol use disorder is unknown. Alcohols 95-102 tumor necrosis factor Homo sapiens 0-22 33680846-3 2020 Tumour necrosis factor (TNF) is a well characterised neuroimmune signal but its involvement in alcohol use disorder is unknown. Alcohols 95-102 tumor necrosis factor Homo sapiens 24-27 33680846-5 2020 Acute ethanol exposure reduces TNF release while chronic alcohol intake generally increases TNF levels. Alcohols 57-64 tumor necrosis factor Homo sapiens 92-95 33680846-6 2020 Evidence suggests TNF potentiates excitatory transmission, promotes anxiety during alcohol withdrawal and is involved in drug use in rodents. Alcohols 83-90 tumor necrosis factor Homo sapiens 18-21 33680846-7 2020 An association between craving for alcohol and TNF is apparent during withdrawal in humans. Alcohols 35-42 tumor necrosis factor Homo sapiens 47-50 33680846-9 2020 Overall, defining TNF"s role in alcohol use disorder is complicated by poor understanding of its variable effects on synaptic transmission and neurogenesis. Alcohols 32-39 tumor necrosis factor Homo sapiens 18-21 33680846-11 2020 Understanding the individual relevance of TNF in alcohol use disorder awaits a more comprehensive understanding of TNF"s effects within the brain. Alcohols 49-56 tumor necrosis factor Homo sapiens 42-45 32963013-4 2020 Mechanistically, alcohol intake increased the engulfment capacity of microglia in a manner dependent on the kinase Src, the subsequent activation of the transcription factor NF-kappaB, and the consequent production of the proinflammatory cytokine TNF. Alcohols 17-24 tumor necrosis factor Homo sapiens 247-250 2648095-0 1989 Alcohol suppresses lipopolysaccharide-induced tumor necrosis factor activity in serum and lung. Alcohols 0-7 tumor necrosis factor Homo sapiens 46-67 34052691-7 2021 RESULTS: There was a significant reduction in TNF-alpha concentration (F [3, 20.42] = 4.96, p = 0.01, eta2p = 0.42) post alcohol administration, compared to baseline concentrations, and a significant increase in IL-6 concentrations (F [3, 27.81] = 9.06, p < 0.001, eta2p = 0.49) post alcohol administration, compared to baseline. Alcohols 121-128 tumor necrosis factor Homo sapiens 46-55 34052691-7 2021 RESULTS: There was a significant reduction in TNF-alpha concentration (F [3, 20.42] = 4.96, p = 0.01, eta2p = 0.42) post alcohol administration, compared to baseline concentrations, and a significant increase in IL-6 concentrations (F [3, 27.81] = 9.06, p < 0.001, eta2p = 0.49) post alcohol administration, compared to baseline. Alcohols 284-291 tumor necrosis factor Homo sapiens 46-55 32942936-8 2020 Furthermore, downregulation of ROCK2 attenuated alcohol-induced inflammation by reducing the levels of pro-inflammatory cytokines (tumor necrosis factor (TNF)-alpha and interleukin (IL)-6) and enhanced the level of anti-inflammatory IL-10. Alcohols 48-55 tumor necrosis factor Homo sapiens 131-164 31759072-0 2020 Acute alcohol consumption alters the peripheral cytokines IL-8 and TNF-alpha. Alcohols 6-13 tumor necrosis factor Homo sapiens 67-76 31759072-10 2020 CONCLUSIONS: In our exploratory data, acute alcohol challenge (120 mg/dL) elicits dynamic changes in the pro-inflammatory molecules IL-8 and TNF-alpha. Alcohols 44-51 tumor necrosis factor Homo sapiens 141-150 31750821-8 2019 The mRNA and protein expression levels of HDAC3 increased in a dose-dependent manner after alcohol treatment at these concentration s. Compared with the control group, TNF-alpha and phosphorylated NF-kappaBp65 levels increased, whereas TER and protein levels of occludin, claudin-1 and IkappaB decreased in the alcohol group. Alcohols 91-98 tumor necrosis factor Homo sapiens 168-177 31750821-9 2019 Compared with the alcohol group, TNF-alpha and phosphorylated NF-kappaBp65 levels were reduced, while TER and protein levels of occludin, claudin-1 and IkappaB were elevated in the alcohol combined with HDAC3 inhibitor group. Alcohols 181-188 tumor necrosis factor Homo sapiens 33-42 30737481-3 2019 Exposure to neonatal alcohol resulted in acute increases in activation and inflammatory gene expression in hypothalamic microglia including tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6). Alcohols 21-28 tumor necrosis factor Homo sapiens 140-167 30737481-3 2019 Exposure to neonatal alcohol resulted in acute increases in activation and inflammatory gene expression in hypothalamic microglia including tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6). Alcohols 21-28 tumor necrosis factor Homo sapiens 169-178 30737481-7 2019 Investigation of possible epigenetic programming mechanisms by alcohol revealed neonatal alcohol decreased several repressive regulators of transcription in hypothalamic microglia, while concomitantly increasing histone H3 acetyl lysine 9 (H3K9ac) enrichment at TNF-alpha and IL-6 promoter regions. Alcohols 89-96 tumor necrosis factor Homo sapiens 262-271 28936843-1 2016 To evaluate the rationality of alcohol precipitation technology of Biqiu granule by investigating its effect on serum histamine, IgE, IL-4, IFN and TNF-alpha. Alcohols 31-38 tumor necrosis factor Homo sapiens 148-157 29445009-5 2018 In vivo and in vitro binge alcohol exposure significantly inhibited the TLR4-MyD88 cytokines TNF-alpha and IL-6, as well as the TLR4-TRIF cytokines/chemokines IFN-beta, IP-10, and RANTES, in human monocytes, but not TLR3-TRIF-induced cytokines/chemokines, as detected by quantitative PCR and ELISA. Alcohols 27-34 tumor necrosis factor Homo sapiens 93-102 28168393-9 2017 Further, alcohol-related increases (1.5-3.0 fold) were observed in the expression of hepatic cytokines (TNF-alpha, IL-1 beta, IL-6, IL-10) and other factors noted to be involved in the colonization of CRC cells including ICAM-1, CCL-2, CCL-7, MMP-2, and MMP-9. Alcohols 9-16 tumor necrosis factor Homo sapiens 104-113 31334440-4 2019 In active drinkers, quantitative real-time polymerase chain reaction revealed alcohol-induced activation of tumor necrosis factor alpha, interleukin (IL)-1beta, and nuclear factor kappa B in liver tissue already at early disease stages. Alcohols 78-85 tumor necrosis factor Homo sapiens 108-135 29113896-1 2018 Excessive alcohol intake induces an inflammatory response in the brain, via TNFalpha, TLR4 and NF-kappaB signaling pathways. Alcohols 10-17 tumor necrosis factor Homo sapiens 76-84 28993831-7 2017 We also noticed successively increasing percentage of TNF A and IL-10 risk haplotypes with life style habits like smoking (10 and 26%) and alcohol consuming (9 and 27%). Alcohols 139-146 tumor necrosis factor Homo sapiens 54-59 28993831-9 2017 We could also notice higher frequency of TNF A and IL-10 risk haplotypes in smoker and alcohol user. Alcohols 87-94 tumor necrosis factor Homo sapiens 41-46 28935932-6 2017 CBD significantly attenuated the alcohol feeding-induced serum transaminase elevations, hepatic inflammation (mRNA expressions of TNFalpha, MCP1, IL1beta, MIP2 and E-Selectin, and neutrophil accumulation), oxidative/nitrative stress (lipid peroxidation, 3-nitrotyrosine formation, and expression of reactive oxygen species generating enzyme NOX2). Alcohols 33-40 tumor necrosis factor Homo sapiens 130-138 27082578-9 2016 Thus, older subjects with increased serum ApoB levels are more likely to present with increased CIMT, suggesting that age and ApoB promote such thickening and that TNFalpha downregulation might play a protective role against the progression of subclinical atherosclerosis in subjects with chronic alcohol consumption. Alcohols 297-304 tumor necrosis factor Homo sapiens 164-172 27256567-11 2016 Alcohol withdrawal partially restored the distribution of monocyte subsets and the frequency of IL-6-producing monocytes and increased the frequency of TNF-producing cells in response to LPS and PGN stimulation to levels compared with those in HC. Alcohols 0-7 tumor necrosis factor Homo sapiens 152-155 26408704-9 2015 The results showed that the AA and AG genotypes of TNFA -308G/A increased HCC susceptibility which was obvious among males, smokers, and alcohol drinkers, but not females, non-smokers, or non-drinkers (p=0.0003, 0.0003, 0.0014, 0.6127, 0.7442 and 0.3010, respectively). Alcohols 137-144 tumor necrosis factor Homo sapiens 51-55 26842246-11 2016 Alcohol pretreatment blocked TACE activity and TNF-alpha release in hog barn dust-treated cells. Alcohols 0-7 tumor necrosis factor Homo sapiens 47-56 25356030-3 2014 Alcohol activates the innate immune system and induces an imbalance of the immune response, which is followed by activated Kupffer cell-derived tumor necrosis factor (TNF)-alpha overproduction, which is in turn responsible for the changes in the hepatic SREBP-1 and PAI-1 activity. Alcohols 0-7 tumor necrosis factor Homo sapiens 144-177 26226164-4 2015 Oral administration of BBR was able to significantly reduce this alcohol-induced damage, inhibit increases of alcohol-induced TNFalpha and IL-1beta expression in gastrointestinal mucosa as well as their upstream signals TLR2 and TLR4, and regulate cytokines that modulate tight junctions. Alcohols 110-117 tumor necrosis factor Homo sapiens 126-134 25262503-0 2014 TNF-alpha and IL-6 serum levels: neurobiological markers of alcohol consumption in alcohol-dependent patients? Alcohols 60-67 tumor necrosis factor Homo sapiens 0-9 25262503-0 2014 TNF-alpha and IL-6 serum levels: neurobiological markers of alcohol consumption in alcohol-dependent patients? Alcohols 83-90 tumor necrosis factor Homo sapiens 0-9 25262503-9 2014 Our results support an association between alterations in TNF-alpha and IL-6 serum levels and alcohol consumption. Alcohols 94-101 tumor necrosis factor Homo sapiens 58-67 25356030-4 2014 Alcohol abuse promotes the migration of bone marrow-derived cells (BMDCs) to the liver and then reprograms TNF-alpha expression from BMDCs. Alcohols 0-7 tumor necrosis factor Homo sapiens 107-116 25356030-5 2014 Chronic alcohol intake triggers the sympathetic hyperactivity-activated hepatic stellate cell (HSC) feedback loop that in turn activates the HSCs, resulting in HSC-derived TNF-alpha overproduction. Alcohols 8-15 tumor necrosis factor Homo sapiens 172-181 24224954-2 2014 Hepatocytes are normally resistant to the cytotoxic effects of TNF, but they become sensitized to TNF by chronic alcohol exposure. Alcohols 113-120 tumor necrosis factor Homo sapiens 98-101 24855832-8 2014 TNF-alpha could sensitize the toxic response of HepG2 cells to those exogenous compounds, indicating the important role of TNF-alpha in the pathogenesis of alcohol, drugs and oxidant related liver diseases. Alcohols 156-163 tumor necrosis factor Homo sapiens 0-9 24855832-8 2014 TNF-alpha could sensitize the toxic response of HepG2 cells to those exogenous compounds, indicating the important role of TNF-alpha in the pathogenesis of alcohol, drugs and oxidant related liver diseases. Alcohols 156-163 tumor necrosis factor Homo sapiens 123-132 24995667-5 2014 RESULTS: Alcohol-use disorders patients with a positive history of MD had higher levels of the inflammatory cytokines IL-6 (P = 0.019), TNF (P = 0.020), and IFN-gamma (P = 0.001), but not of IL-10 (P = 0.853). Alcohols 9-16 tumor necrosis factor Homo sapiens 136-139 25024384-6 2014 In vitro pre-exposure to moderate alcohol reduced subsequent LPS-induced NF-kappaB promoter activity and downstream TNF-alpha, IL-6 and IL-1beta production in monocytes and macrophages, exhibiting endotoxin tolerance. Alcohols 34-41 tumor necrosis factor Homo sapiens 116-125 25024384-7 2014 Mechanistic analysis demonstrates that alcohol-induced HSF1 binds to the TNF-alpha promoter in macrophages at early time points, exerting transrepression and decreased TNF-alpha expression. Alcohols 39-46 tumor necrosis factor Homo sapiens 73-82 25024384-7 2014 Mechanistic analysis demonstrates that alcohol-induced HSF1 binds to the TNF-alpha promoter in macrophages at early time points, exerting transrepression and decreased TNF-alpha expression. Alcohols 39-46 tumor necrosis factor Homo sapiens 168-177 24224954-1 2014 BACKGROUND: Chronic alcohol exposure results in liver injury that is driven in part by inflammatory cytokines such as tumor necrosis factor-alpha (TNF). Alcohols 20-27 tumor necrosis factor Homo sapiens 118-145 24224954-1 2014 BACKGROUND: Chronic alcohol exposure results in liver injury that is driven in part by inflammatory cytokines such as tumor necrosis factor-alpha (TNF). Alcohols 20-27 tumor necrosis factor Homo sapiens 147-150 23618528-0 2013 Lactobacillus rhamnosus GG reduces hepatic TNFalpha production and inflammation in chronic alcohol-induced liver injury. Alcohols 91-98 tumor necrosis factor Homo sapiens 43-51 24091659-5 2013 Alcohol exposure enhanced acinar cell-specific production of TNFalpha, IL-6, MCP-1 and IL-10, as early as 3 h after LPS, whereas IL-18 and caspase-1 were evident 24 h later. Alcohols 0-7 tumor necrosis factor Homo sapiens 61-69 24091659-6 2013 Alcohol enhanced LPS-induced TNFalpha expression, whereas blockade of LPS signaling diminished TNFalpha production in vitro, indicating that the response of pancreatic acinar cells to LPS is similar to that of immune cells. Alcohols 0-7 tumor necrosis factor Homo sapiens 29-37 23618528-12 2013 In conclusion, probiotic LGG treatment reduced alcohol-induced hepatic inflammation by attenuation of TNFalpha production via inhibition of TLR4- and TLR5-mediated endotoxin activation. Alcohols 47-54 tumor necrosis factor Homo sapiens 102-110 22420891-7 2012 Low and moderate alcohol consumption led to lower TNF-alpha levels: 2.92 (1.79-4.63), 2.83 (1.84-4.48), 2.82 (1.76-4.34) and 3.15 (1.91-4.73) pg/ml for nondrinkers, low, moderate and high drinkers, respectively, p<0.02, and this difference remained borderline significant (p=0.06) after multivariate adjustment. Alcohols 17-24 tumor necrosis factor Homo sapiens 50-59 22902304-0 2012 Genetic variants of TNFalpha, IL10, IL1beta, CTLA4 and TGFbeta1 modulate the indices of alcohol-induced liver injury in East Indian population. Alcohols 88-95 tumor necrosis factor Homo sapiens 20-28 22782967-4 2012 We found that acute alcohol pretreatment resulted in the same attenuating effect as LPS pretreatment on TLR4-induced TNF-alpha production in human monocytes and murine RAW 264.7 macrophages. Alcohols 20-27 tumor necrosis factor Homo sapiens 117-126 24080827-0 2013 ER stress activating ATF4/CHOP-TNF-alpha signaling pathway contributes to alcohol-induced disruption of osteogenic lineage of multipotential mesenchymal stem cell. Alcohols 74-81 tumor necrosis factor Homo sapiens 31-40 24080827-13 2013 CONCLUSION: Our data therefore revealed a role of ER stress and ATF4/CHOP in the ethanol-induced inhibition of osteogenesis, and activation of TNF-alpha signaling by ATF4/CHOP linking ER stress to adipogenic lineage in response to alcohol stimulation. Alcohols 231-238 tumor necrosis factor Homo sapiens 143-152 24080827-14 2013 This work should establish a new signaling pathway linking alcohol, ER stress, and TNF-alpha to loss of bone formation: Ethanol ER stress ATF4 & CHOP TNF-alpha Osteoblasts . Alcohols 59-66 tumor necrosis factor Homo sapiens 166-175 24080828-1 2013 BACKGROUND/AIMS: We have reported in a separate study that alcohol exposure triggers activation of the TNF-alpha signaling pathway leading to an adverse shift of multipotential mesenchymal stem cells in bone marrow (BMSCs) away from osteogenesis towards adipogenesis. Alcohols 59-66 tumor necrosis factor Homo sapiens 103-112 24080828-3 2013 Here we showed that in addition to promoting the TNF-alpha signaling, alcohol also suppressed the Wnt1/beta-catenin signaling pathway. Alcohols 70-77 tumor necrosis factor Homo sapiens 49-58 22841563-0 2012 Alcohol depletes coenzyme-Q(10) associated with increased TNF-alpha secretion to induce cytotoxicity in HepG2 cells. Alcohols 0-7 tumor necrosis factor Homo sapiens 58-67 22420891-10 2012 CONCLUSIONS: Moderate alcohol consumption is associated with lower levels of IL-6 and (to a lesser degree) of TNF-alpha, irrespective of the type of alcohol consumed. Alcohols 22-29 tumor necrosis factor Homo sapiens 110-119 22969921-8 2012 Further stratified analyses showed that after stratification for history of alcohol drinking, in a subgroup of individuals without a history of drinking, the HCC risk in the group with the TNF-alpha rs1800630 A allele was 1.839 times higher than that in the group with TNF-alpha rs1800630 C (P<0.010). Alcohols 76-83 tumor necrosis factor Homo sapiens 189-198 22028977-4 2012 Considerable attention has been given to alcohol elevated production of lipopolysaccharide (LPS) and TNFalpha and to alcohol induction of CYP2E1. Alcohols 41-48 tumor necrosis factor Homo sapiens 101-109 21097658-12 2011 Caregivers showed increased concentrations of TNF-alpha with alcohol use relative to good sleepers. Alcohols 61-68 tumor necrosis factor Homo sapiens 46-55 21731903-2 2011 Alcohol consumption results in translocation of gut bacteria into the portal system along with lipopolysaccharides that interact with toll-like receptors and results in the production of inflammatory and immunogenic mediators such as tumor necrosis factor-alpha (TNF-alpha) and interferons. Alcohols 0-7 tumor necrosis factor Homo sapiens 234-261 21731903-2 2011 Alcohol consumption results in translocation of gut bacteria into the portal system along with lipopolysaccharides that interact with toll-like receptors and results in the production of inflammatory and immunogenic mediators such as tumor necrosis factor-alpha (TNF-alpha) and interferons. Alcohols 0-7 tumor necrosis factor Homo sapiens 263-272 21731903-3 2011 Chronic consumption of alcohol causes priming of this process in which there is enhanced production of cytokines, interferon, interleukins, and TNF-alpha. Alcohols 23-30 tumor necrosis factor Homo sapiens 144-153 21962237-8 2011 Acute alcohol inhibited TLR8- or TLR4-induced TNF alpha protein and mRNA induction while it augmented IL-10 production in monocytes. Alcohols 6-13 tumor necrosis factor Homo sapiens 46-55 21962237-9 2011 In contrast, prolonged alcohol treatment augmented TNF alpha without affecting IL-10 production significantly in response to either TLR8 or TLR4 ligand stimulation. Alcohols 23-30 tumor necrosis factor Homo sapiens 51-60 21143255-12 2011 CONCLUSIONS: Alcohol interferes with the kinetics of Foxp3, RORgammat, and T-bet gene expression and the production of TNF-alpha and IL-1ss and influences the balance of Treg/Th17 cells following LPS exposure. Alcohols 13-20 tumor necrosis factor Homo sapiens 119-128 20843633-7 2011 Increasing carbon chain length of straight chain alcohols positively correlated with their ability to inhibit detection of tumor necrosis factor alpha (TNF-alpha) and interleukin 10 (IL-10), but not with the detection of interleukin 6 (IL-6), interleukin 8, (IL-8), and interleukin 12 (IL-12). Alcohols 49-57 tumor necrosis factor Homo sapiens 123-150 20843633-7 2011 Increasing carbon chain length of straight chain alcohols positively correlated with their ability to inhibit detection of tumor necrosis factor alpha (TNF-alpha) and interleukin 10 (IL-10), but not with the detection of interleukin 6 (IL-6), interleukin 8, (IL-8), and interleukin 12 (IL-12). Alcohols 49-57 tumor necrosis factor Homo sapiens 152-161 19561104-2 2009 We hypothesized that in human monocytes, acute alcohol induces hyporesponsiveness to LPS, resulting in decreased TNF-alpha, whereas chronic alcohol increases TNF-alpha by sensitization to LPS. Alcohols 47-54 tumor necrosis factor Homo sapiens 113-122 19798529-4 2010 Considerable attention has been given to alcohol-elevated production of lipopolysaccharide (LPS) and TNFalpha and to alcohol induction of CYP2E1. Alcohols 41-48 tumor necrosis factor Homo sapiens 101-109 27713249-5 2010 This age-related increase of ME-Dif was exaggerated by regular alcohol drinking and beta-blocker use. Alcohols 63-70 tumor necrosis factor Homo sapiens 32-35 27713249-7 2010 AZ treatment decreased age-related increase in ME-Dif particularly in patients who were regular consumers of alcohol and in beta-blocker users. Alcohols 109-116 tumor necrosis factor Homo sapiens 50-53 19185287-2 2009 This study was undertaken to test whether blockade of biologically active tumor necrosis factor-alpha (TNF-alpha) normalizes REM sleep in alcohol-dependent adults. Alcohols 138-145 tumor necrosis factor Homo sapiens 74-101 19185287-2 2009 This study was undertaken to test whether blockade of biologically active tumor necrosis factor-alpha (TNF-alpha) normalizes REM sleep in alcohol-dependent adults. Alcohols 138-145 tumor necrosis factor Homo sapiens 103-112 19185287-8 2009 CONCLUSIONS: Pharmacologic neutralization of TNF-alpha activity is associated with significant reductions in REM sleep in abstinent alcohol-dependent patients. Alcohols 132-139 tumor necrosis factor Homo sapiens 45-54 19561104-2 2009 We hypothesized that in human monocytes, acute alcohol induces hyporesponsiveness to LPS, resulting in decreased TNF-alpha, whereas chronic alcohol increases TNF-alpha by sensitization to LPS. Alcohols 140-147 tumor necrosis factor Homo sapiens 158-167 19561104-6 2009 Inhibition of IRAK-M in acute alcohol-exposed monocytes using small interfering RNA restored the LPS-induced TNF-alpha production whereas over-expression of IRAK-M in chronic alcohol macrophages prevented the increase in TNF-alpha production. Alcohols 30-37 tumor necrosis factor Homo sapiens 109-118 19561104-6 2009 Inhibition of IRAK-M in acute alcohol-exposed monocytes using small interfering RNA restored the LPS-induced TNF-alpha production whereas over-expression of IRAK-M in chronic alcohol macrophages prevented the increase in TNF-alpha production. Alcohols 175-182 tumor necrosis factor Homo sapiens 221-230 19032584-4 2009 Tumor necrosis factor-alpha (TNF-alpha) produced in response to alcohol exposure may cause fatty liver by up-regulating SREBP-1 activity, whereas betaine and pioglitazone may attenuate fatty liver by down-regulating SREBP-1 activity. Alcohols 64-71 tumor necrosis factor Homo sapiens 0-27 19135070-6 2009 An activator of NF-kappaB, tumor necrosis factor-alpha (TNF-alpha), protected immature cerebellar granule neuron cultures against alcohol-induced cell death in a dose-dependent fashion. Alcohols 130-137 tumor necrosis factor Homo sapiens 27-54 19135070-6 2009 An activator of NF-kappaB, tumor necrosis factor-alpha (TNF-alpha), protected immature cerebellar granule neuron cultures against alcohol-induced cell death in a dose-dependent fashion. Alcohols 130-137 tumor necrosis factor Homo sapiens 56-65 19135070-11 2009 TNF-alpha reduced the alcohol vulnerability of immature neurons, while NFi increased the vulnerability of mature neurons. Alcohols 22-29 tumor necrosis factor Homo sapiens 0-9 19032584-4 2009 Tumor necrosis factor-alpha (TNF-alpha) produced in response to alcohol exposure may cause fatty liver by up-regulating SREBP-1 activity, whereas betaine and pioglitazone may attenuate fatty liver by down-regulating SREBP-1 activity. Alcohols 64-71 tumor necrosis factor Homo sapiens 29-38 18689673-0 2008 Alcohol exposure regulates heat shock transcription factor binding and heat shock proteins 70 and 90 in monocytes and macrophages: implication for TNF-alpha regulation. Alcohols 0-7 tumor necrosis factor Homo sapiens 147-156 18689673-2 2008 Alteration of inflammatory responses by alcohol is linked to dysregulated TNF-alpha production. Alcohols 40-47 tumor necrosis factor Homo sapiens 74-83 18689673-12 2008 Inhibition of hsp90 using geldanamycin prevented prolonged alcohol-induced elevation in LPS-induced NF-kappaB and TNF-alpha production. Alcohols 59-66 tumor necrosis factor Homo sapiens 114-123 18689673-14 2008 Further, hsp90 regulates TNF-alpha production in macrophages contributing to alcohol-induced inflammation. Alcohols 77-84 tumor necrosis factor Homo sapiens 25-34 18449625-1 2008 Liver is a prime target of alcohol-induced damage by inducing inflammatory cytokines especially tumor necrosis factor alpha (TNFalpha). Alcohols 27-34 tumor necrosis factor Homo sapiens 96-123 18579335-0 2008 Serum TNF-alpha levels in relation to alcohol consumption and common TNF gene polymorphisms. Alcohols 38-45 tumor necrosis factor Homo sapiens 6-15 18579335-0 2008 Serum TNF-alpha levels in relation to alcohol consumption and common TNF gene polymorphisms. Alcohols 38-45 tumor necrosis factor Homo sapiens 6-9 18579335-1 2008 Tumor necrosis factor-alpha (TNF-alpha) mediates alcohol-induced organ dysfunction, including alcoholic hepatitis. Alcohols 49-56 tumor necrosis factor Homo sapiens 0-27 18579335-1 2008 Tumor necrosis factor-alpha (TNF-alpha) mediates alcohol-induced organ dysfunction, including alcoholic hepatitis. Alcohols 49-56 tumor necrosis factor Homo sapiens 29-38 18579335-4 2008 The study was aimed at investigating the level of serum TNF-alpha levels in adults and analyzing its relationship with different levels of alcohol consumption, as well as the potential interaction between alcohol consumption and common TNF-alpha gene polymorphisms in relation to TNF-alpha levels and liver disease. Alcohols 139-146 tumor necrosis factor Homo sapiens 56-65 18449625-1 2008 Liver is a prime target of alcohol-induced damage by inducing inflammatory cytokines especially tumor necrosis factor alpha (TNFalpha). Alcohols 27-34 tumor necrosis factor Homo sapiens 125-133 18580445-0 2008 Polymorphisms of the TNF, CD14, and HSPA1B genes in patients with acute alcohol-induced pancreatitis. Alcohols 72-79 tumor necrosis factor Homo sapiens 21-24 18822146-10 2008 Integrating these pieces of information our model shows how excessive alcohol use would be expected to lead to reduced TNF signaling, reduced MTHFR expression, and increased susceptibility to depression. Alcohols 70-77 tumor necrosis factor Homo sapiens 119-122 17980786-6 2007 Alcohol-induced endothelial damage or protection may be related to the synthesis or action of several markers, such as nitric oxide, cortisol, endothelin-1, adhesion molecules, tumor necrosis factor alpha, interleukin-6, C-reactive protein, and haemostatic factors. Alcohols 0-7 tumor necrosis factor Homo sapiens 177-204 18312327-0 2008 Tumour necrosis factor (TNF-alpha) alpha converting enzyme and soluble TNF-alpha receptor type 1 in psoriasis patients in relation to the chronic alcohol consumption. Alcohols 146-153 tumor necrosis factor Homo sapiens 24-33 18312327-0 2008 Tumour necrosis factor (TNF-alpha) alpha converting enzyme and soluble TNF-alpha receptor type 1 in psoriasis patients in relation to the chronic alcohol consumption. Alcohols 146-153 tumor necrosis factor Homo sapiens 71-80 18312327-4 2008 The aim of the study was to analyse the relationship between long-term alcohol consumption and the concentration of TACE in peripheral blood mononuclear cells (PBMC) and its substrate--soluble TNF-alpha receptor type 1 (sTNF-R1) in plasma in psoriasis patients. Alcohols 71-78 tumor necrosis factor Homo sapiens 193-202 18045675-3 2008 Moreover, by inducing mitochondrial alterations, oxidative stress promotes hepatocyte necrosis and contributes to alcohol-induced sensitization of hepatocyte to the pro-apoptotic action of TNF-alpha. Alcohols 114-121 tumor necrosis factor Homo sapiens 189-198 18198478-9 2007 TNF-alpha and free radicals are produced in early alcohol-induced liver injury. Alcohols 50-57 tumor necrosis factor Homo sapiens 0-9 18198478-10 2007 In support of this finding, the pathology caused by alcohol was blocked nearly completely in TNF-alpha receptor 1. Alcohols 52-59 tumor necrosis factor Homo sapiens 93-102 17266151-3 2007 METHODS: Spontaneous and in vitro-stimulated production of interleukin (IL) 1alpha (TNFalpha) by PB monocytes was analyzed at the single level by flow cytometry in chronic alcoholics without liver disease and active ethanol (EtOH) intake (AWLD group), as well as in patients with alcohol liver cirrhosis (ALC group), who were either actively drinking (ALCET group) or with alcohol withdrawal (ALCAW group). Alcohols 172-179 tumor necrosis factor Homo sapiens 84-92 17854140-7 2007 Important humoral factors, including adiponectin, and tumor necrosis factor-alpha (TNF-alpha), also regulate alcohol-induced steatosis. Alcohols 109-116 tumor necrosis factor Homo sapiens 54-81 17854140-7 2007 Important humoral factors, including adiponectin, and tumor necrosis factor-alpha (TNF-alpha), also regulate alcohol-induced steatosis. Alcohols 109-116 tumor necrosis factor Homo sapiens 83-92 17889312-6 2007 Concentrations of tumor necrosis factor-alpha and monocyte chemoattractant protein-1 in BALF in the alcohol consumption group were increased. Alcohols 100-107 tumor necrosis factor Homo sapiens 18-45 17900056-1 2007 AIMS: In our work, the factors affecting the plasma level of cytokine, tumour necrosis factor (TNF-alpha) and liver function tests values in alcohol dependent males after alcohol abuse period were analysed. Alcohols 141-148 tumor necrosis factor Homo sapiens 95-104 17900056-8 2007 CONCLUSION: Values of TNF-alpha and liver function tests two weeks after alcohol withdrawal were independently determined by gastric pH, H.pylori infection and smoking, which suggests their potential synergism with a hepatotoxic effect of alcohol drinking. Alcohols 73-80 tumor necrosis factor Homo sapiens 22-31 17900056-8 2007 CONCLUSION: Values of TNF-alpha and liver function tests two weeks after alcohol withdrawal were independently determined by gastric pH, H.pylori infection and smoking, which suggests their potential synergism with a hepatotoxic effect of alcohol drinking. Alcohols 239-246 tumor necrosis factor Homo sapiens 22-31 17321745-5 2007 Further, we found that incorporation of unsaturation in the alcohol moiety increases the potential of the compound for the inhibition of TNF-alpha induced expression of ICAM-1 and also for the inhibition of lipid peroxidation. Alcohols 60-67 tumor necrosis factor Homo sapiens 137-146 16916584-0 2006 Interleukin-1 alpha and beta, TNF-alpha and HTTLPR gene variants study on alcohol toxicity and detoxification outcome. Alcohols 74-81 tumor necrosis factor Homo sapiens 30-39 17592223-4 2007 METHODS: The effects of acute or chronic alcohol exposure were evaluated in human monocytes on the production of TNFalpha or IL-10 production, pro-inflammatory gene and nuclear factor-kappaB (NF-kappaB) activation. Alcohols 41-48 tumor necrosis factor Homo sapiens 113-121 17592223-5 2007 RESULTS: Moderate, acute alcohol consumption or equivalent doses of alcohol in vitro had anti-inflammatory effects on monocyte activation via inhibition of pro-inflammatory genes and NF-kappaB activation, inhibition of TNFalpha production and augmentation of the anti-inflammatory cytokine, IL-10. Alcohols 25-32 tumor necrosis factor Homo sapiens 219-227 17592223-6 2007 In contrast, acute alcohol treatment augmented NF-kappaB activation and TNFalpha production and inhibited IL-10 levels in the presence of complex stimulation with combined TLR2 and TLR4 ligands. Alcohols 19-26 tumor necrosis factor Homo sapiens 72-80 17592223-7 2007 Prolonged alcohol exposure also resulted in an increase in NF-kappaB and TNFalpha production in response to TLR4 stimulation with LPS. Alcohols 10-17 tumor necrosis factor Homo sapiens 73-81 16958667-5 2006 Mitochondrial GSH depletion due to alcohol-mediated alteration in mitochondrial membrane dynamics underlies the susceptibility of hepatocytes from alcohol-fed models to tumor necrosis factor (TNF), and in nutritional and genetic models of hepatic steatosis, mGSH depletion occurs due to the enrichment of mitochondria in free cholesterol, resulting in decreased mitochondrial membrane fluidity. Alcohols 35-42 tumor necrosis factor Homo sapiens 169-190 16958667-5 2006 Mitochondrial GSH depletion due to alcohol-mediated alteration in mitochondrial membrane dynamics underlies the susceptibility of hepatocytes from alcohol-fed models to tumor necrosis factor (TNF), and in nutritional and genetic models of hepatic steatosis, mGSH depletion occurs due to the enrichment of mitochondria in free cholesterol, resulting in decreased mitochondrial membrane fluidity. Alcohols 35-42 tumor necrosis factor Homo sapiens 192-195 16958667-5 2006 Mitochondrial GSH depletion due to alcohol-mediated alteration in mitochondrial membrane dynamics underlies the susceptibility of hepatocytes from alcohol-fed models to tumor necrosis factor (TNF), and in nutritional and genetic models of hepatic steatosis, mGSH depletion occurs due to the enrichment of mitochondria in free cholesterol, resulting in decreased mitochondrial membrane fluidity. Alcohols 147-154 tumor necrosis factor Homo sapiens 169-190 16873800-5 2006 Odds of elevated IL-6 and TNF-alpha (>75th percentile) were, respectively, 1.95 (95% CI 1.56-2.44) and 1.88 (1.51-2.35) for diabetic participants and 1.51 (1.21-1.87) and 1.14 (0.92-1.42) for those with IFG/IGT after adjustment for age, sex, race, smoking, alcohol intake, education, and study site. Alcohols 260-267 tumor necrosis factor Homo sapiens 26-35 16313198-8 2005 The structure-activity studies indicate that the chain length of the alcohol moiety, substituents in the aromatic ring, and alpha, beta-double bond of the cinnamic acid ester have significant effects on the inhibition of TNF-alpha-induced expression of ICAM-1 on endothelial cells. Alcohols 69-76 tumor necrosis factor Homo sapiens 221-230 16751410-3 2006 In human monocytes, alcohol attenuated TLR4- but not TLR2-induced TNF-alpha protein and mRNA levels and NF-kappaB activation. Alcohols 20-27 tumor necrosis factor Homo sapiens 66-75 16751410-4 2006 In contrast, acute alcohol augmented TNF-alpha production when both TLR2 and TLR4 ligands were present. Alcohols 19-26 tumor necrosis factor Homo sapiens 37-46 16433741-8 2006 RESULTS: Eighteen hours after moderate alcohol consumption, we found a significant reduction in monocyte production of inflammatory mediators, TNF-alpha and IL-1beta, in response to LPS or staphylococcal enterotoxin B stimulation. Alcohols 39-46 tumor necrosis factor Homo sapiens 143-152 16433741-9 2006 Acute alcohol consumption inhibited LPS-induced DNA binding of the p65/p50 NF-kappaB in monocytes that regulates the expression of both the TNF-alpha and the IL-1beta genes. Alcohols 6-13 tumor necrosis factor Homo sapiens 140-149 16923312-5 2006 The available evidence indicates that, by favouring mitochondrial permeability transition, oxidative stress promotes hepatocyte necrosis and/or apoptosis and is implicated in the alcohol-induced sensitization of hepatocytes to the pro-apoptotic action of TNF-alpha. Alcohols 179-186 tumor necrosis factor Homo sapiens 255-264 16751410-10 2006 Consistent with this result, the JNK inhibitor prevented alcohol-induced augmentation of TNF-alpha production. Alcohols 57-64 tumor necrosis factor Homo sapiens 89-98 16132116-3 2005 However, the direct effect of alcohol in the induction of IL-1beta and TNF-alpha has not been clarified. Alcohols 30-37 tumor necrosis factor Homo sapiens 71-80 16344602-2 2005 One of the key processes mediating the progression of ALD involved the overproduction of tumor necrosis factor (TNF) and the susceptibility of hepatocytes to TNF-induced apoptosis by alcohol intake. Alcohols 183-190 tumor necrosis factor Homo sapiens 158-161 16344602-6 2005 The depletion of mGSH by alcohol has been described to determine the susceptibility of hepatocytes to TNF-mediated cell death. Alcohols 25-32 tumor necrosis factor Homo sapiens 102-105 16246259-0 2005 Alcohol reversibly disrupts TNF-alpha/TACE interactions in the cell membrane. Alcohols 0-7 tumor necrosis factor Homo sapiens 28-37 16246259-2 2005 One cellular mechanism responsible for this effect is alcohol-induced suppression of TNF-alpha (TNF) by mononuclear phagocytes. Alcohols 54-61 tumor necrosis factor Homo sapiens 85-94 16246259-2 2005 One cellular mechanism responsible for this effect is alcohol-induced suppression of TNF-alpha (TNF) by mononuclear phagocytes. Alcohols 54-61 tumor necrosis factor Homo sapiens 85-88 16246259-3 2005 We have previously shown that alcohol in part inhibits TNF-alpha processing by TNF converting enzyme (TACE) in human monocytes. Alcohols 30-37 tumor necrosis factor Homo sapiens 55-64 16246259-3 2005 We have previously shown that alcohol in part inhibits TNF-alpha processing by TNF converting enzyme (TACE) in human monocytes. Alcohols 30-37 tumor necrosis factor Homo sapiens 55-58 16246259-4 2005 We hypothesized that the chain length of the alcohol is critical for post-transcriptional suppression of TNF secretion. Alcohols 45-52 tumor necrosis factor Homo sapiens 105-108 15845418-6 2005 Depletion of mitochondrial GSH by alcohol is believed to contribute to the sensitization of the liver to alcohol-induced injury through tumor necrosis factor (TNF)-mediated hepatocellular death. Alcohols 34-41 tumor necrosis factor Homo sapiens 136-157 16205374-8 2005 The presentations were (1) Innate Immune responses of Alcohol-exposed mice and macrophage-like cells following infections with Listeria monocytogenes by Robert T. Cook 2) Alcohol, cytokines and host defense by Kyle Happel 3) Decreased antigen presentation and anergy induced by alcohol in myeloid dendritic cells by Pranoti Mandrekar 4) Transcriptional regulation of TNF-alpha in human monocytes by chronic ethanol: role of the cellular redox state by Jay Kolls 5) Estrogen and gender differences in inflammatory responses after alcohol and burn injury by Elizabeth Kovacs. Alcohols 54-61 tumor necrosis factor Homo sapiens 367-376 16170395-20 2005 This suggests that alcohol may modulate the inhibitory effect of TNF-alpha on AN production, and thus, increase its plasma concentrations. Alcohols 19-26 tumor necrosis factor Homo sapiens 65-74 15845418-6 2005 Depletion of mitochondrial GSH by alcohol is believed to contribute to the sensitization of the liver to alcohol-induced injury through tumor necrosis factor (TNF)-mediated hepatocellular death. Alcohols 34-41 tumor necrosis factor Homo sapiens 159-162 15845418-6 2005 Depletion of mitochondrial GSH by alcohol is believed to contribute to the sensitization of the liver to alcohol-induced injury through tumor necrosis factor (TNF)-mediated hepatocellular death. Alcohols 105-112 tumor necrosis factor Homo sapiens 136-157 15845418-6 2005 Depletion of mitochondrial GSH by alcohol is believed to contribute to the sensitization of the liver to alcohol-induced injury through tumor necrosis factor (TNF)-mediated hepatocellular death. Alcohols 105-112 tumor necrosis factor Homo sapiens 159-162 15609483-4 2004 Among the polymorphic genes and environmental interactions discussed with respect to prenatal development are those for P-glycoprotein (multidrug resistance protein) and the avermectins; methylenetetrahydrofolate reductase (MTHFR), an enzyme in folate metabolism, and dietary folic acid; transforming growth factor alpha (TGFalpha) and cigarette smoke; and alcohol dehydrogenase (ADH) and cytochrome P-450 (CYP) 2E1 in association with alcohol consumption. Alcohols 357-364 tumor necrosis factor Homo sapiens 288-320 16054986-5 2005 In addition, the accumulation of iron in hepatic macrophage isolated from laboratory animals chronically ingesting alcohol is associated with activation of nuclear factor-kappa B and production of tumor necrosis factor-alpha, providing a proinflammatory cellular environment also favorable for initiation and promotion of carcinogenesis. Alcohols 115-122 tumor necrosis factor Homo sapiens 197-224 15288835-6 2004 After controlling for age and use of alcohol and tobacco, the TNF-alpha/sTNF-RII ratio showed significant differences comparing OSCC patients at each treatment stage with normal controls. Alcohols 37-44 tumor necrosis factor Homo sapiens 62-71 15902922-6 2004 Increased serum TNF-alpha concentrations were specifically found in heavy drinkers with the -857 (C-->T) substitution (CT heterozygotes), therefore indicating an interaction between alcohol consumption and that polymorphism on serum TNF-alpha concentrations. Alcohols 185-192 tumor necrosis factor Homo sapiens 16-25 15596091-1 2004 Tumor necrosis factor-alpha (TNF-alpha) is one of a number of cytokines implicated in the progression of alcohol-induced liver disease. Alcohols 105-112 tumor necrosis factor Homo sapiens 0-27 15596091-1 2004 Tumor necrosis factor-alpha (TNF-alpha) is one of a number of cytokines implicated in the progression of alcohol-induced liver disease. Alcohols 105-112 tumor necrosis factor Homo sapiens 29-38 15188512-1 2004 AIM: To clarify whether -238G/A polymorphism of tumor necrosis factor-alpha (TNF-alpha) gene promoter region was associated with outcomes of hepatitis B virus (HBV) infection in Han population of northern China, and to analyze the gene-environment interaction between -238G/A polymorphism and cigarette smoking or alcohol consumption. Alcohols 314-321 tumor necrosis factor Homo sapiens 77-86 15157952-5 2004 Coupled with prolonged sleep latency and increased rapid eye movement sleep, alcoholics showed nocturnal elevations of IL-6 and TNF as compared to controls after adjustment for alcohol consumption and body mass index. Alcohols 77-84 tumor necrosis factor Homo sapiens 128-131 15353169-2 2004 Tumor necrosis factor-alpha (TNF-alpha) constitutes a major factor in the development of alcohol-induced liver injury. Alcohols 89-96 tumor necrosis factor Homo sapiens 0-27 15353169-2 2004 Tumor necrosis factor-alpha (TNF-alpha) constitutes a major factor in the development of alcohol-induced liver injury. Alcohols 89-96 tumor necrosis factor Homo sapiens 29-38 15353169-3 2004 In alcohol-dependent subjects, elevated levels of plasma TNF-alpha are strongly predictive of mortality. Alcohols 3-10 tumor necrosis factor Homo sapiens 57-66 14693987-3 2004 Moderate alcohol consumption may increase adiponectin, which in turn causes a decrease of tumor necrosis factor (TNF)-alpha. Alcohols 9-16 tumor necrosis factor Homo sapiens 90-123 11991856-7 2002 These acute-alcohol-induced changes in monocytic cells were different compared to T lymphocytes, both in Jurkat CD4 cells and peripheral human T cells, acute alcohol had a biphasic effect on TNF-alpha-induced NF-kappa B activation via an I-kappa B alpha-dependent mechanism. Alcohols 12-19 tumor necrosis factor Homo sapiens 191-200 15041894-5 2003 Tumor necrosis factor-alpha (TNF-alpha) has emerged as a key player in the progression of the alcohol-induced liver disease (ALD), and is known to target mitochondria. Alcohols 94-101 tumor necrosis factor Homo sapiens 0-27 15041894-5 2003 Tumor necrosis factor-alpha (TNF-alpha) has emerged as a key player in the progression of the alcohol-induced liver disease (ALD), and is known to target mitochondria. Alcohols 94-101 tumor necrosis factor Homo sapiens 29-38 15041894-7 2003 In experimental models alcohol consumption enhances cholesterol levels and subsequent deposition into mitochondria resulting in selective decrease in the mGSH stores which is sufficient by itself to sensitize hepatocytes to TNF-alpha-mediated cell death. Alcohols 23-30 tumor necrosis factor Homo sapiens 224-233 15041894-8 2003 Thus, the combination of TNF-alpha overproduction, enhanced glycosphingolipid generation and selective mGSH depletion by alcohol intake cooperate making the liver sensitive to alcohol. Alcohols 176-183 tumor necrosis factor Homo sapiens 25-34 12436048-14 2002 Further, these results demonstrate that acute alcohol is a potent inhibitor of NF-kappaB activation by mediators of early (LPS) or late (IL-1, TNF(alpha)) stages of inflammation in monocytes. Alcohols 46-53 tumor necrosis factor Homo sapiens 143-153 12626543-0 2003 Acute alcohol inhibits TNF-alpha processing in human monocytes by inhibiting TNF/TNF-alpha-converting enzyme interactions in the cell membrane. Alcohols 6-13 tumor necrosis factor Homo sapiens 23-32 12626543-0 2003 Acute alcohol inhibits TNF-alpha processing in human monocytes by inhibiting TNF/TNF-alpha-converting enzyme interactions in the cell membrane. Alcohols 6-13 tumor necrosis factor Homo sapiens 23-26 12626543-2 2003 One cellular mechanism responsible for this effect is alcohol-induced suppression of TNF-alpha by mononuclear phagocytes. Alcohols 54-61 tumor necrosis factor Homo sapiens 85-94 12626543-3 2003 We undertook experiments to better understand the cellular mechanisms by which alcohol dose-dependently suppresses TNF elaboration by human monocytes. Alcohols 79-86 tumor necrosis factor Homo sapiens 115-118 12626543-4 2003 Here we show in human primary monocytes and cell lines that alcohol suppresses LPS-induced TNF secretion post-transcriptionally by inhibiting cellular processing by TNF-alpha-converting enzyme (TACE). Alcohols 60-67 tumor necrosis factor Homo sapiens 91-94 12626543-5 2003 Using fluorescent resonance energy transfer microscopy, physiological relevant levels of alcohol resulted in a reversible dose-dependent decrease in fluorescent resonance energy transfer efficiency between TNF and TACE. Alcohols 89-96 tumor necrosis factor Homo sapiens 206-209 12626543-6 2003 These data demonstrate that alcohol inhibits interactions between TNF and its converting enzyme, TACE, possibly by affecting membrane fluidity. Alcohols 28-35 tumor necrosis factor Homo sapiens 66-69 12436048-9 2002 RESULTS: Our results indicate that acute alcohol inhibits IL-1beta- and TNFalpha-induced NF-kappaB activation. Alcohols 41-48 tumor necrosis factor Homo sapiens 72-80 12436048-11 2002 Inhibition of NF-kappaB by acute alcohol was concomitant with decreased levels of the IkappaB(alpha) molecule in the cytoplasm of LPS, IL-1, and TNFalpha-activated monocytes. Alcohols 33-40 tumor necrosis factor Homo sapiens 145-153 12107045-3 2002 RESULTS: Increased leptin plasma levels in alcohol addicts correlated significantly with an enhanced secretion of TNF-alpha, which was itself related to the duration of alcohol misuse. Alcohols 43-50 tumor necrosis factor Homo sapiens 114-123 12107045-3 2002 RESULTS: Increased leptin plasma levels in alcohol addicts correlated significantly with an enhanced secretion of TNF-alpha, which was itself related to the duration of alcohol misuse. Alcohols 169-176 tumor necrosis factor Homo sapiens 114-123 12062638-12 2002 Finally, generation of reactive oxygen species (which occurs during alcohol metabolism) and products of lipid peroxidation induce production of cytokines, such as TNF and IL-8. Alcohols 68-75 tumor necrosis factor Homo sapiens 163-166 11991856-7 2002 These acute-alcohol-induced changes in monocytic cells were different compared to T lymphocytes, both in Jurkat CD4 cells and peripheral human T cells, acute alcohol had a biphasic effect on TNF-alpha-induced NF-kappa B activation via an I-kappa B alpha-dependent mechanism. Alcohols 158-165 tumor necrosis factor Homo sapiens 191-200 11091023-16 2000 Among the cytokines, IL-1beta, IL-6, and TNFalpha were the predominant cytokines affected by chronic use of alcohol during pregnancy. Alcohols 108-115 tumor necrosis factor Homo sapiens 41-49 11505050-6 2001 RESULTS: In HepG2 cells, both IFNalpha and acute alcohol treatment induced NF-kappaB activation and augmented TNFalpha-induced NF-kappaB binding. Alcohols 49-56 tumor necrosis factor Homo sapiens 110-118 11552332-3 2001 Alcohol acts as an immunosuppressor in different ways, namely through suppression of TNF synthesis. Alcohols 0-7 tumor necrosis factor Homo sapiens 85-88 11091023-20 2000 We conclude that chronic alcohol use during pregnancy stimulated the fetal cytokine synthesis and secretion, and IL-1beta, IL-6, and TNF alpha were the predominant cytokines affected by alcohol. Alcohols 186-193 tumor necrosis factor Homo sapiens 133-142 9622433-4 1998 In this study, we investigated the effects of chronic alcohol consumption on alveolar macrophage release of TNFalpha in vitro. Alcohols 54-61 tumor necrosis factor Homo sapiens 108-116 10619810-2 2000 This study examined the separate and combined effects of in vivo lentiviral infection and in vitro alcohol exposure on alveolar macrophage (AM) production of tumor necrosis factor- alpha (TNF-alpha), a proinflammatory cytokine that is critical to normal pulmonary host defense. Alcohols 99-106 tumor necrosis factor Homo sapiens 158-186 10619810-2 2000 This study examined the separate and combined effects of in vivo lentiviral infection and in vitro alcohol exposure on alveolar macrophage (AM) production of tumor necrosis factor- alpha (TNF-alpha), a proinflammatory cytokine that is critical to normal pulmonary host defense. Alcohols 99-106 tumor necrosis factor Homo sapiens 188-197 9214463-2 1997 Tumor necrosis factor alpha (TNF-alpha) has emerged as the "final common pathway" in the pathogenesis of alcohol-related hepatic necro-inflammation. Alcohols 105-112 tumor necrosis factor Homo sapiens 0-27 9622433-13 1998 We conclude that chronic alcohol consumption significantly suppresses LPS-stimulated alveolar macrophage production of TNFalpha. Alcohols 25-32 tumor necrosis factor Homo sapiens 119-127 9622433-15 1998 Because TNFalpha production is an important element in host defense, this may explain, in part, the susceptibility of chronic alcohol abusers to a variety of infections. Alcohols 126-133 tumor necrosis factor Homo sapiens 8-16 9391290-6 1997 RESULTS: Serum TNF alpha concentrations were positively related to body mass index and Helicobacter pylori infection, but inversely related to alcohol consumption. Alcohols 143-150 tumor necrosis factor Homo sapiens 15-24 9214463-2 1997 Tumor necrosis factor alpha (TNF-alpha) has emerged as the "final common pathway" in the pathogenesis of alcohol-related hepatic necro-inflammation. Alcohols 105-112 tumor necrosis factor Homo sapiens 29-38 8986216-6 1996 Both acute and chronic alcohol consumption of ethanol increase hepatic expression of TNF alpha. Alcohols 23-30 tumor necrosis factor Homo sapiens 85-94 8865966-3 1996 Our data show that in vitro treatment of blood monocytes with a physiologically relevant dose of alcohol (25 mM) results in significantly decreased induction of tumor necrosis factor-alpha (TNF alpha) and interleukin (IL)-1 beta by bacterial stimulation of either Gram-positive [staphylococcal enterotoxin B (SEB), 1 microgram/ml of SEB] or Gram-negative [lipopolysaccharide (LPS), 1 microgram/ml of LPS] origin both at the protein and mRNA levels. Alcohols 97-104 tumor necrosis factor Homo sapiens 161-188 8865966-3 1996 Our data show that in vitro treatment of blood monocytes with a physiologically relevant dose of alcohol (25 mM) results in significantly decreased induction of tumor necrosis factor-alpha (TNF alpha) and interleukin (IL)-1 beta by bacterial stimulation of either Gram-positive [staphylococcal enterotoxin B (SEB), 1 microgram/ml of SEB] or Gram-negative [lipopolysaccharide (LPS), 1 microgram/ml of LPS] origin both at the protein and mRNA levels. Alcohols 97-104 tumor necrosis factor Homo sapiens 190-199 8807202-0 1996 Alcohol inhibits lipopolysaccharide-induced tumor necrosis factor alpha gene expression by peripheral blood mononuclear cells as measured by reverse transcriptase PCR in situ hybridization. Alcohols 0-7 tumor necrosis factor Homo sapiens 44-71 8807202-1 1996 We recently showed that alcohol significantly suppressed lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-alpha) production by whole blood and total mononuclear cells from healthy subjects as measured by bioassay. Alcohols 24-31 tumor necrosis factor Homo sapiens 119-128 8807202-1 1996 We recently showed that alcohol significantly suppressed lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-alpha) production by whole blood and total mononuclear cells from healthy subjects as measured by bioassay. Alcohols 24-31 tumor necrosis factor Homo sapiens 90-117 8807202-2 1996 In the current study, we further examined the effect of alcohol on LPS-induced TNF-alpha gene expression by semiquantitative solution PCR and in situ reverse transcriptase PCR (RT-PCR) hybridization methods. Alcohols 56-63 tumor necrosis factor Homo sapiens 79-88 8807202-6 1996 In solution RT-PCR in vitro analysis, alcohol significantly suppressed TNF-specific message. Alcohols 38-45 tumor necrosis factor Homo sapiens 71-74 8807202-7 1996 In conventional in situ hybridization, the effect of alcohol on TNF-alpha gene expression was poorly detected. Alcohols 53-60 tumor necrosis factor Homo sapiens 64-73 8807202-8 1996 However, when cells were subjected to RT-PCR prior to in situ hybridization, cells treated with alcohol significantly suppressed expression of the message for TNF-alpha. Alcohols 96-103 tumor necrosis factor Homo sapiens 159-168 8807202-9 1996 These studies confirm our earlier finding that alcohol suppressed the production of TNF-alpha by LPS-induced whole blood cells and peripheral blood mononuclear cells. Alcohols 47-54 tumor necrosis factor Homo sapiens 84-93 1320807-0 1992 Effect of acute alcohol administration on TNF-alpha binding to neutrophils and isolated liver plasma membranes. Alcohols 16-23 tumor necrosis factor Homo sapiens 42-51 7541951-1 1995 Alcohol (EtOH) has been shown to suppress lipopolysaccharide (LPS)-induced nitric oxide (NO) generation and tumor necrosis factor (TNF) production in the lung in vivo. Alcohols 0-7 tumor necrosis factor Homo sapiens 108-129 7541951-1 1995 Alcohol (EtOH) has been shown to suppress lipopolysaccharide (LPS)-induced nitric oxide (NO) generation and tumor necrosis factor (TNF) production in the lung in vivo. Alcohols 0-7 tumor necrosis factor Homo sapiens 131-134 8730220-8 1996 Data presented in this study demonstrate that: (1) acute alcohol consumption can alter the kinetic behavior of IL-6 and TNF-alpha in the bloodstream, mainly by accelerating their clearance which, in turn, may counteract the outcome of cytokine secretion and delivery to the blood; and (2) short exposure of liver to ethanol levels commonly seen in humans after binge drinking may alter its capacity to take up cytokines. Alcohols 57-64 tumor necrosis factor Homo sapiens 120-129 7883861-2 1994 We found that, unlike non-alcohol-exposed patients, patients with acute alcohol use prior to trauma have a transient decrease in monocyte tumor necrosis factor alpha (TNF alpha) production during the very early postinjury (0-3 days) period. Alcohols 72-79 tumor necrosis factor Homo sapiens 138-165 7883861-2 1994 We found that, unlike non-alcohol-exposed patients, patients with acute alcohol use prior to trauma have a transient decrease in monocyte tumor necrosis factor alpha (TNF alpha) production during the very early postinjury (0-3 days) period. Alcohols 72-79 tumor necrosis factor Homo sapiens 167-176 7883861-3 1994 However, TNF alpha production by these alcohol-exposed patients" monocytes (M0) became hyperelevated late postinjury (> 9 days). Alcohols 39-46 tumor necrosis factor Homo sapiens 9-18 7883861-4 1994 Consequently, these massively elevated M0 TNF alpha levels can contribute to posttrauma immunosuppression after acute alcohol use. Alcohols 118-125 tumor necrosis factor Homo sapiens 42-51 7883861-7 1994 Both SEB- and LPS-induced TNF alpha mRNA induction was inhibited by acute alcohol treatment in normal M0, indicating that ethanol can regulate cytokine gene expression. Alcohols 74-81 tumor necrosis factor Homo sapiens 26-35 1995437-9 1991 These data suggest that tumor necrosis factor-alpha and interleukin-1 alpha are related to some of the metabolic consequences of both acute and chronic alcohol-induced liver disease, whereas interleukin-6 is related to abnormalities seen in acute liver injury. Alcohols 152-159 tumor necrosis factor Homo sapiens 24-51 25346502-9 2014 RESULTS: The expression of TLR2, TRAF-6, NF-kappaB p65, and the proinflammatory cytokines, TNF-alpha and IL-6, were significantly increased after alcohol exposure in EA.hy926 endothelial cells. Alcohols 146-153 tumor necrosis factor Homo sapiens 91-100 34827151-6 2021 Conditioned macrophages with serum obtained after four-week intervention with alcohol-free beer significantly reduced the transcription of pro-inflammatory interleukins such as IL-1beta and TNF. Alcohols 78-85 tumor necrosis factor Homo sapiens 190-193 34676244-9 2021 In-depth analyses suggested that MT1H may be more applicable to alcohol-derived HCC and involved in the downregulation of the inflammatory pathway, Jak-STAT pathway, TNF pathway, and Wnt signaling pathway. Alcohols 64-71 tumor necrosis factor Homo sapiens 166-169 35611350-6 2022 Alcohol use (positive phosphatidylethanol level) was associated with elevated IFN-gamma, tumor necrosis factor alpha (TNF-alpha), and interleukin 12p70 (IL-12p70), and smoking was associated with higher macrophage inflammatory protein 1alpha, TNF-alpha, and IL-12p70. Alcohols 0-7 tumor necrosis factor Homo sapiens 89-116 35611350-6 2022 Alcohol use (positive phosphatidylethanol level) was associated with elevated IFN-gamma, tumor necrosis factor alpha (TNF-alpha), and interleukin 12p70 (IL-12p70), and smoking was associated with higher macrophage inflammatory protein 1alpha, TNF-alpha, and IL-12p70. Alcohols 0-7 tumor necrosis factor Homo sapiens 118-127 35611350-6 2022 Alcohol use (positive phosphatidylethanol level) was associated with elevated IFN-gamma, tumor necrosis factor alpha (TNF-alpha), and interleukin 12p70 (IL-12p70), and smoking was associated with higher macrophage inflammatory protein 1alpha, TNF-alpha, and IL-12p70. Alcohols 0-7 tumor necrosis factor Homo sapiens 243-252 34475376-0 2021 Predictive values of tumor necrosis factor-alpha for depression treatment outcomes: effect modification by hazardous alcohol consumption. Alcohols 117-124 tumor necrosis factor Homo sapiens 21-48 34475376-3 2021 The aim of the present study was to investigate the effects of the serum tumor necrosis factor-alpha (sTNF-alpha) level on antidepressant treatment outcomes in terms of the 12-week and 12-month remission rates and 24-month relapse rate, and to investigate the potential modifying effects of alcohol consumption on these associations in patients with depressive disorders. Alcohols 291-298 tumor necrosis factor Homo sapiens 73-100 35371104-5 2022 Alcohol-use disorder was associated with evidence of advanced innate immune activation, alterations in monocyte phenotype including increased expression of Toll-like receptor 4, increased burden of stimulatory ligands for Toll-like receptor 4, and alterations in plasma cytokine signature, most notably elevations in soluble CD40 ligand and transforming growth factor beta. Alcohols 0-7 tumor necrosis factor Homo sapiens 341-372