Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human milk has been shown to contain numerous immune components that can potentially protect the infant during the period before its own immune system is completely developed. Alcohol consumption in both experimental animals and humans has been associated with alterations to a number of immune parameters. We have investigated the possibility that alcohol consumption during pregnancy alters certain immune components in day 3 postpartum breast milk and peripheral blood of women. Our study group consisted of 10 alcoholic beverage drinkers (moderate to heavy, most of whom smoked a 1/2-1 pack of cigarettes per day), 15 non-drinking/non-smoking controls, and 10 non-drinking/smokers (1/2-1 pack per day) controls. The immune parameters measured in these otherwise healthy women were: (1) percentage and absolute number of the various subsets of leukocytes; (2) percentage of T cells, B cells, T helper and cytotoxic/suppressors subsets, and natural killer cells; (3) levels of the cytokines IL-6, IL-8 and TNF-alpha; (4) levels of IgA in milk and IgG in serum. Milk from the alcohol group contained an elevated amount of IL-8 as compared with milk from non-smoker controls; however, it did not differ statistically from that of the smoker controls. Blood from the alcohol group showed an increased level of IL-8 when compared with that from both smoker and non-smoker controls. The total number of leukocytes in milk was elevated in milk from the alcohol group as compared to both the smoker and non-smoker control groups. In the leukocyte component of milk, neutrophils predominate and are responsible for the elevation in total number of cells, as both lymphocyte and macrophage populations did not differ from those of the controls. For lymphocytes, B cells were also increased in blood of the smokers as compared with the alcohol and non-smokers controls. There were no statistical differences in any of the other immune parameters tested among the three groups. The present study found that alcohol consumption during pregnancy could modulate the production of IL-8 and infiltration of certain leukocytes in milk and blood of postpartum women. Some of these alterations were also evident in the smoker controls and thus could not be attributed to alcohol consumption alone.
Alcohol Alcohol
PMID:Preliminary study of how alcohol consumption during pregnancy affects immune components in breast milk and blood of postpartum women. 937

There is increased activity of the proinflammatory cytokine, tumor necrosis factor (TNF) in alcoholic liver disease (ALD). Hepatic neutrophil infiltration is a principal injurious manifestation of ALD. TNF can induce cellular oxidative injury directly, and indirectly by inducing neutrophil chemotactic factor (IL-8) production by hepatocytes. IL-8 activates and chemotactically attracts neutrophils to the liver where they release oxidizing substances. Patients with ALD also have decreased protective factors for cellular oxidative injury. Manganous superoxide dismutase (MnSOD) is an antioxidant protective factor. The objectives of these studies were to investigate mechanisms for induction of an injurious factor (IL-8) and a protective factor (MnSOD) in the HepG2 human hepatoma cell line. In the first set of experiments, IL-8 gene reporter constructs were used to transiently transfect a derivative (MVh2E1-9) of the HepG2 cell line which expresses P-4502E1 and metabolizes ethanol. Inactivation of the NF-kappaB and 3'NF-IL-6 DNA binding sites decreased IL-8 gene transcriptional activation in response to TNF while inactivation of the 5'NF-IL-6 binding site increased IL-8 gene transcriptional activity in response to TNF. This system may be useful to assess the effects of ethanol on TNF-induced hepatocyte IL-8 production. In the second set of experiments, HepG2 cells were cultured in 25 to 100 mmol concentrations of ethanol. Both TNF and ethanol increased HepG2 cell MnSOD activity in short-term (72 hr) cultures with ethanol. However, after long-term (10 weeks) culture with ethanol, there was no induction of MnSOD by ethanol and there was a diminished induction of MnSOD in response to TNF. Further studies are needed to assess the effect of this diminished induction of MnSOD with chronic ethanol culture on HepG2 cell susceptibility to TNF cytotoxicity. We conclude that transfected liver cell lines can be used to evaluate mechanisms for increased injurious factors and decreased protective factors in alcoholic liver injury.
Alcohol Clin Exp Res 1998 Jun
PMID:Use of transfected liver cells to evaluate potential mechanisms of alcohol-induced liver injury. 966 Feb 98

Interleukin-8 (IL-8), an inflammatory cytokine that promotes neutrophil accumulation, has been implicated in the pathogenesis of alcoholic liver disease but the mechanism of its production is unknown. The ability of lipid peroxidation products, also implicated in alcoholic liver disease, to stimulate IL-8 production was studied because of their alleged role in alcoholic liver disease. Peroxidized fatty acids (arachidonic and linolenic) as well as microsomal membranes stimulated IL-8 production by peripheral blood monocytes whereas ethanol and acetaldehyde did not. Hydrocortisone (5 microg/ml) prevented the IL-8 stimulation by peroxidized fatty acids. Ethanol-induced lipid peroxidation may secondarily further alcohol-induced liver injury through IL-8 chemotaxis of neutrophils.
Alcohol 1998 Aug
PMID:Stimulation of monocyte interleukin-8 by lipid peroxidation products: a mechanism for alcohol-induced liver injury. 966 13

Granulocyte colony-stimulating factor (G-CSF) has immunomodulating properties that could be beneficial for adjunctive treatment of severe infections. Cytokine release from stimulated whole blood and expression of neutrophil surface and apoptosis markers in response to G-CSF were studied in human volunteers under physiologic conditions and after ethanol pretreatment. Levels of interleukin (IL)-1 receptor antagonist and soluble tumor necrosis factor (TNF) receptor-1 were significantly increased after G-CSF, whereas TNF-alpha and IL-10 concentrations were reduced, and IL-1beta and IL-8 remained unchanged. There was a significant inhibition of neutrophil apoptosis and increased expression of complement regulatory protein CD55 without changes in CD11b, CD14, and CD59 expression. These effects were well preserved after ethanol pretreatment, which per se led to an increase in apoptosis and decreased CD55 expression. Thus, G-CSF treatment was associated with a reduction of the proinflammatory cytokine response and enhanced neutrophil survival in vivo, suggesting a therapeutic potential of G-CSF for severe infections in the nonneutropenic host.
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PMID:Inhibition of neutrophil apoptosis and modulation of the inflammatory response by granulocyte colony-stimulating factor in healthy and ethanol-treated human volunteers. 972 67

Our clinical and experimental research results indicated the possibility that gut-derived endotoxin contributes to the development of alcoholic liver disease. Long-term ethanol consumption resulted in an enhanced secretory function of hepatic macrophage accompanied by an ultrastructural feature of activation. The liver of rats fed on ethanol-diet were found to have an enhanced ability to produce CINC-1 (rat IL-8) after endotoxin injection. This chemokine may contribute to neutrophil recruitment into the liver in alcoholic liver injury. Females exhibited a greater ability to produce CINC-1 than males, and this fact may account for the gender difference in susceptibility to alcohol-related liver disease.
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PMID:[A pivotal role of activated hepatic macrophage in the progression of alcoholic liver disease]. 1020 91

Evidence suggests a link between alcohol consumption, psoriasis and the response of psoriatic patients to methotrexate (MTX) therapy. Ethanol (EtOH) may play a role in the pathogenesis of psoriasis by upregulating the expression and inducing the local secretion of proinflammatory cytokines, e.g. interleukins IL-1alpha, IL-6, chemokine IL-8 and tumor necrosis factor alpha (TNF-alpha). We investigated whether EtOH or MTX or their combination influence the secretion of these cytokines using normal human primary skin cells (NHPSC) and epidermoid cell line A431. The objectives of this study were: (1) to quantify the differences in cellular changes induced by MTX, (2) to measure the effect of EtOH on MTX toxicity and (3) to determine the relationship between MTX and EtOH exposure and production of proinflammatory cytokines. NHPSC and A431 were incubated with 0-10 mM MTX or alpha-MEM (control) in the presence or absence of 40 mM EtOH. A formazan 3-(4,5-dimethylthiazole-2-yl)-2, 5-diphenyl-tetrazolium bromide (MTT) assay was used as a marker for cell viability (control was 100%). Significance was calculated by ANOVA. Cytokine release into media was quantitated by ELISA. After 24 h of MTX exposure, the release of IL-1alpha was unchanged. IL-6 increased 1.7 times in both cultures, and IL-8 increased 1.7 times in NHPSC and 2.1 times in A431. TNF-alpha release increased twice in A431 but not in NHPSC. Human recombinant IL-1alpha and IL-6 for 24 h had no effect, while TNF-alpha reduced cytoviability by 30% in NHPSC and 22% in A431. Anti-TNF-alpha reversed the effect produced by TNF-alpha in NHPSC and reduced it in A431 (11.8%, p < 0.05). We concluded that in vitro in normal human primary keratinocytes, toxicity and inflammatory responses are enhanced by EtOH.
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PMID:Ethanol-modulated cytokine production and expression in skin cells exposed to methotrexate. 1032 85

Acute ethanol (EtOH) intoxication has been identified as a risk factor for infectious complications in trauma and burn victims. However, the mechanism of this immune dysfunction has yet to be elucidated. The monocyte/macrophage production of cytokines, in particular IL-8 and TNF-alpha, is critical in the regulation of the acute inflammatory response to infectious challenge. IL-8 is a potent chemoattractant and activator of neutrophils. TNF-alpha, a proinflammatory cytokine, initiates expression of endothelial cell surface adhesion molecules and neutrophil migration. p38, a member of the mitogen-activated protein kinases, plays an important role in mediating intracellular signal transduction in endotoxin-induced inflammatory responses. We examined the effects of LPS and ethanol on p38 activation and the corresponding IL-8 and TNF-alpha production in human mononuclear cells. LPS-induced IL-8 and TNF-alpha production was inhibited in a similar pattern by pretreatment with either EtOH or SB202190 (1 microM), a specific inhibitor of p38 kinase. Western blot analysis, using a dual phospho-specific p38 mitogen-activated protein kinase Ab, demonstrated that EtOH pretreatment inhibited LPS-induced p38 activation. These results demonstrate that alcohol suppresses the normal host immune inflammatory response to LPS. This dysregulation appears to be mediated in part via inhibition of p38 activation. Inhibition of IL-8 and TNF-alpha production by acute EtOH intoxication may inhibit inflammatory focused neutrophil migration and activation and may be a mechanism explaining the increased risk of trauma- and burn-related infections.
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PMID:Alcohol (ethanol) inhibits IL-8 and TNF: role of the p38 pathway. 1035 98

Interleukin-8 (IL-8), a cytokine produced by a host of cells including monocytes, macrophages, Kupffer cells and hepatocytes, can activate neutrophils. Peripheral neutrophilia and liver neutrophil infiltration are frequently noted in patients with alcoholic liver disease (ALD). Serum IL-8 levels are markedly elevated in patients with alcoholic hepatitis compared with those in patients with alcoholic cirrhosis, alcoholic fatty liver and non-alcoholic liver disease. The levels are also elevated in patients who die of hepatic failure and correlate with biochemical and histologic parameters and severity of liver injury. Patients with high serum IL-8 had a higher mortality rate than those with lower levels. In liver tissue from patients with ALD, local IL-8 levels also correlated with the degree of neutrophil infiltration. Serum IL-8 levels decreased gradually with abstinence from alcohol. Ethanol can increase plasma endotoxin, a potent inducer of tumor necrosis factor (TNF)-alpha and IL-1. Subsequently, TNF-alpha and IL-1, together with endotoxin, stimulate circulating and local IL-8 in ALD. Activated IL-8 then mediates neutrophil infiltration, a pivotal process in the pathogenesis of ALD. IL-8 levels might reflect the stage and severity of ALD and might serve as a predictor of survival in patients with alcoholic hepatitis. The development of agents with an anti-IL-8 effect is promising for the therapy of ALD.
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PMID:Interleukin-8 and alcoholic liver disease. 1041 75

Bovine beta-Lactoglobulin (BLG) was cleaved by BNPS-skatole (2-(2'-nitrophenylsulfenyl)-3-methyl-3'-bromoindolenine), trypsin, or pepsin in 40% ethanol before emulsification with hexadecane in order to characterize the peptides active at the interfaces. The total digests and the different phases obtained after emulsification were analyzed by RP-HPLC to separate the peptides according to their gradual order on a hydrophilicity-to-hydrophobicity scale. In each case, hydrophobic peptides were recovered in the creamed phase and characterized by mass spectrometry and sequencing. After tryptic hydrolysis, short peptides were identified at the interfacial layer as fragments S21-L32, V41-L57, V41-K60, and W61-K70 linked to L149-I162 by a C66-C160 bond. It indicates that the hydrophilic/hydrophobic distribution of the amino acids in the sequence of the fragments is more relevant to adsorption than the length of the peptide. BNPS-skatole and peptic hydrolysis produced larger hydrophobic peptides which were also recovered in the creamed phase of the emulsion and characterized.
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PMID:Emulsification of chemical and enzymatic hydrolysates of beta-lactoglobulin: characterization of the peptides adsorbed at the interface. 1079 74

Cytokine balance alterations are responsible for some of the systemic and hepatic manifestations of alcoholism. The present study was aimed to evaluate the influence of both acute alcohol abstinence (in alcoholics) and acute alcohol intake (in healthy subjects) on serum IL-6, IL-8, IL-10, and IL-12 levels. Serum cytokine concentrations were determined on admission and after a median of 6 days of ethanol abstinence in 29 patients with alcohol withdrawal syndrome. The same determinations were made in five healthy volunteers at baseline and after 36 h of a single 60 g-dose alcohol intake. Increased serum levels of IL-6, IL-10 and, to a lesser extent IL-8, declined in the few days after alcohol abstinence in patients with alcohol withdrawal syndrome. Serum IL-8 values increased after alcohol intake in healthy subjects. Rapid variation of serum cytokine levels along with alcohol intake or abstinence should be taken into account in cytokine studies in alcohol abusers.
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PMID:Influence of acute alcohol intake and alcohol withdrawal on circulating levels of IL-6, IL-8, IL-10 and IL-12. 1097 10


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