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)

Extracellular glutathione deficiency and exaggerated oxidative stress may contribute to the pathogenesis of fibrosing alveolitis (FA). High-dose N-acetylcysteine (NAC) supplementation partially reverses extracellular glutathione depletion and oxidative damage, but effects on intracellular glutathione are unknown. Intracellular total glutathione (GSHt) and activation of bronchoalveolar lavage cells (BAC) obtained from 18 FA patients (9 males, aged 52+/-2 yrs), before and after 12 weeks of oral NAC (600 mg t.i.d.), were assessed. Eight healthy nonsmokers (2 males, aged 36+/-6 yrs) served as a control group. Intracellular GSHt was decreased in FA (1.57+/-0.20 nmol 1x10(6) BAC(-1) versus 2.78+/-0.43 nmol x 10(6) BAC(-1)). After NAC treatment, the intracellular GSHt content increased (1.57+/-0.20 versus 1.87+/-0.19 nmol x 1 x 10(6) BAC(-1)). The spontaneous oxidative activity of BAC decreased after NAC treatment (2.7+/-0.8 versus 1.0+/-0.2 nmol x 1 x 10(6) BAC(-1) x h(-1)). Interleukin-8 concentration (82.1+/-31.5 versus 80.0+/-22.6 pg x mL bronchoalveolar fluid (BALF), nonsignificant (NS)) and myeloperoxidase activity (1.93+/-0.64 versus 1.55+/-0.47 mU x mL(-1) BALF, NS) did not change significantly, but were found to be inversely correlated to intracellular GSHt. In conclusion, high-dose N-acetylcysteine supplementation increases intracellular glutathione levels slightly. This increase is associated with a mild reduction of oxidative activity but not with a reduction of bronchoalveolar cell activation in these patients.
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PMID:Intracellular glutathione and bronchoalveolar cells in fibrosing alveolitis: effects of N-acetylcysteine. 1203 Jul 32

In childhood asthma, cough is a major symptom in some but not in others. There is only limited data on the frequency, severity and prevalence of cough in children with classical asthma. Studies have largely shown no relationship between cough frequency and cough receptor sensitivity with various asthma severity indices. However relating cough severity with asthma severity is limited by various methodological and sensitivity issues, and these are presented in this paper. Mild asthma exacerbations in a group of children with cough as a dominant symptom were characterised by an increase in cough severity (daytime cough scores) and eosinophilic inflammation but not neutrophilic inflammation. However neither cough receptor sensitivity or cough scores related to airway IL-8, eosinophil cationic protein, myeloperoxidase or serum eosinophil cationic protein, and, asthma scores consistently related to cough score only early in the asthma exacerbation phase.
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PMID:Relationship between cough, cough receptor sensitivity and asthma in children. 1209 81

This paper lists the genotype frequencies of 50 polymorphisms of 37 genes (ALDH2, ADRB2, ADRB3, COMT, CD36, CXCR2, CCND1, COX2, CYP2A6, CYP17, CYP19, IGF1, IL-1A, IL-1B, IL-1RN, IL-1R1, IL-6, IL-8, IL-10, LEP, Le, L-myc, MPO, MTR, MTHFR, MAO-A, NQO1, OGG1, p53, p73, Se, SRD5A2, TGF-B, TNF-A, TNF-B, XPD, and XRCC1) and 6 sets of combined genotype frequencies for 241 non-cancer Japanese outpatients. Though the genotype frequencies of 25 polymorphisms have already been reported in our previous papers, 15 polymorphisms (CD36 A52C, CXCR2 C785T, CCND1 G870A, IGF1 C/T at intron 2 and G2502T, IL-1A 46-bp VNTR, IL-1R1 C-116T, IL-6 Ins/Del 17C, IL-8 A-278T and C74T, IL- 10 T-819C, LEP A-2548G, SRD5A2 2-bp VNTR, XPD Lys751Gln, and XRCC1 Arg399Gln) and six sets of combined genotype frequencies (IL-1B C-31T and IL-1A C-889T, IL-1B C-31T and IL-1RN 86-bp VNTR, IL-1B C-31T and IL-1R1 C-116T, TNF-A G-308A and TNF-B A252G, SRD5A2 Val89Leu and 2-bp VNTR, and XRCC1 Arg399Gln and XPD Lys751Gln) were reported in this paper for the first time for Japanese. Although microarray technology will produce this kind of information in near future, this is the first document that reports the genotype/allele frequencies among Japanese for an archival purpose.
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PMID:Genotype frequencies of 50 polymorphisms for 241 Japanese non-cancer patients. 1216 25

The lipid mediator PAF plays an important role in the phagocytosis of particles, including bacteria, and consequent production of pro-inflammatory cytokines, such as TNF-alpha and IL-8. Using a PAF receptor antagonist (UK-74,505) and PAF receptor knock-out mice, we have investigated the relevance of PAF for the inflammatory changes and lethality after pulmonary infection with the gram-negative bacteria Klebsiella pneumoniae in mice. At an inoculum of 3 x 10(6) bacteria, there was marked pulmonary (bronchoalveolar lavage and lung) neutrophilia that started early (2.5 h after infection) and peaked at 48 h. All animals were dead by day 4 of infection. The chemokine KC and the pro-inflammatory cytokine TNF-alpha increased rapidly and persisted for 48 h in the lungs. Pretreatment with UK-74,505 (30 mg kg(-1) per day, p.o.) had no significant effects on the number of infiltrating neutrophils in BAL fluid or lung tissue, as assessed by histology and measuring myeloperoxidase, or on the concentrations of KC. In contrast, concentrations of TNF-alpha and the number of bacteria inside neutrophils were significantly diminished. In order to support a role for the PAF during K. pneumoniae infection, experiments were also carried out in PAFR-deficient mice. In the latter animals, lethality occurred earlier than in wild-type controls. This was associated with greater number of bacteria in lung tissue and diminished percentage of neutrophils containing bacteria in their cytoplasm. Our results suggest that PAF, acting on its receptor, plays a protective role during infection with K. pneumoniae in mice.
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PMID:Role of the platelet-activating factor (PAF) receptor during pulmonary infection with gram negative bacteria. 1238 75

Chronic obstructive pulmonary disease (COPD) is characterized by chronic obstruction of expiratory flow affecting peripheral airways, associated with chronic bronchitis (mucus hypersecretion with goblet cell and submucosal gland hyperplasia) and emphysema (destruction of airway parenchyma), together with fibrosis and tissue damage, and inflammation of the small airways. Cytokines are extracellular signalling proteins. Increased levels of interleukin (IL)-6, IL-1beta, tumour necrosis factor-alpha (TNF-alpha) and IL-8 have been measured in sputum, with further increases during exacerbations, and the bronchiolar epithelium over-expresses monocyte chemotactic protein (MCP)-1 and IL-8. IL-8 can account for some chemotactic activity of sputum, and sputum IL-8 levels correlate with airway bacterial load and blood myeloperoxidase levels. The expression of chemokines such as regulated on activation, normal T-cell expressed and secreted (RANTES) may underlie the airway eosinophilia observed in some COPD patients. Cytokines may be involved in tissue remodelling. TNF-alpha and IL-1beta stimulate macrophages to produced matrix metalloproteinase-9 (MMP-9), and bronchial epithelial cells to produce extracellular matrix glycoproteins such as tenascin. Increased expression of transforming growth factor-beta (TGFbeta) and of epidermal growth factor (EGF) occurs in the epithelium and submucosal cells of patients with chronic bronchitis. TGFbeta and EGF activate proliferation of fibroblasts, while activation of the EGF receptor leads to mucin gene expression. The cytokine profile seen in chronic obstructive pulmonary disease is different from that observed in asthma. The role of these cytokines needs to be defined and there is a potential for anticytokine therapy in chronic obstructive pulmonary disease.
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PMID:Cytokines in chronic obstructive pulmonary disease. 1239 35

Taurine chloramine (TauCl), a product of neutrophil myeloperoxidase - halide system, formed by a reaction of taurine with HOCl, is known as an anti-microbial and anti-inflammatory long-lived oxidant. We previously reported that TauCl inhibits in vitro the production of proinflammatory cytokines (IL-6, IL-8) by RA synoviocytes. Therefore we performed this study to investigate the effect of TauCl treatment on the development of collagen-induced arthritis (CIA) in DBA1/J mice. Early administration of TauCl (after primary immunization) resulted in the delay of the onset of CIA, but had no effect on severity of arthritis. TauCl, given daily for 21 days after booster immunization, did not reduce the symptoms of arthritis in those mice, which already developed CIA, but significantly diminished incidence of the disease (55% vs. 90% of placebo mice). The mechanism of this effect is unknown. This is the first in vivo study suggesting that TauCl may be used for immune intervention in chronic inflammatory diseases.
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PMID:Effect of taurine chloramine, the product of activated neutrophils, on the development of collagen-induced arthritis in DBA 1/J mice. 1243 10

In bronchoalveolar lavage (BAL) fluid from ventilated patients, cytotoxic oxidant activity is correlated with neutrophil activation. The aim of the present study was to investigate the hypothesis that BAL fluid induces activation of the transcription nuclear factor-kappaB (NF-kappaB) in human alveolar cells, in correlation with inflammatory mediators. We measured endotoxin, inflammatory cytokines [interleukin-1beta (IL-1beta), IL-8], nitrated proteins and the activity of myeloperoxidase (MPO) in BAL fluid from ventilated patients developing bronchopneumonia ( n =19 samples) or with acute respiratory distress syndrome (ARDS) ( n =14), and from ARDS/infection-free patients ( n =11). We also exposed alveolar cells to the BAL fluid or to human MPO, H(2)O(2) or HOCl, and tested nuclear extracts for the activation of NF-kappaB. IL-1beta, IL-8, nitrated protein, MPO and endotoxin levels were significantly higher in BAL fluid from patients with bronchopneumonia than in that from the ARDS and ARDS/infection-free groups. A correlation was observed between IL-8 and MPO values ( r =0.82). The level of NF-kappaB activity induced by the BAL fluid was correlated with levels of IL-1beta ( P <0.001), IL-8 ( P <0.005) and MPO ( P <0.002), and with the neutrophil count ( P <0.002), and was higher for BAL fluid from the bronchopneumonia group. NF-kappaB activation by MPO was also demonstrated. The activation of NF-kappaB by BAL fluid, especially that from bronchopneumonia patients, suggests that a similar phenomenon may occur in vivo, leading to potential amplification of the inflammatory reaction.
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PMID:Bronchoalveolar lavage fluids of patients with lung injury activate the transcription factor nuclear factor-kappaB in an alveolar cell line. 1244 10

To date, there has been little research examining how elevated ambient temperatures exert an additional effect on the acute immune response to endurance exercise. Seven endurance-trained, non-heat-acclimated men [mean (95% confidence interval): 29.7 (25.9-33.5) years, .VO(2max) 66.3 (61.3-71.3) ml.kg(-1).min(-1)] performed two 60-min treadmill runs (75% .VO(2max)) in two different environments (EX1: 18 degrees C/50% room temperature/relative humidity and EX2: 28 degrees C/50% room temperature/relative humidity) with a 7-day interval between the runs. Blood samples were drawn at rest and 0, 0.5, 3, 24, and 48 h after exercise. Compared to EX1, exercise-induced increases in core temperature, sweating rate, heart rate, plasma norepinephrine, cortisol, human growth hormone, and neutrophil and monocyte counts were significantly (5% level) more pronounced after EX2. In contrast, responses of plasma epinephrine, myeloperoxidase, interleukin (IL)-6 as well as lymphocyte counts were similar in EX1 and EX2. Plasma concentrations of IL-8 and C-reactive protein were affected by neither exercise nor by additional heat exposure. Our results suggest that the additional impact of elevated ambient temperatures on stress responses to endurance exercise in trained subjects seems to affect primarily the cardiocirculatory and hormonal systems, and resulting changes in neutrophil and monocyte cell-trafficking. In contrast, heat stress does not seem to exert large additional effects on the acute immune response to endurance exercise as performed in the present study.
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PMID:Impact of elevated ambient temperatures on the acute immune response to intensive endurance exercise. 1273 44

In-vitro data suggest that long-acting beta2-agonists may have a neutrophil-stabilising effect. A reduction in airway wall eosinophil number following introduction of salmeterol in persistent asthma has previously been described. There is currently interest in the "neutrophil system" in asthma, and thus the aim of the present study was to investigate the effect of salmeterol on interleukin (IL)-8, neutrophils and myeloperoxidase (MPO) in persistent asthma. In the same 12-week double-blind parallel-group placebo-controlled study as described previously, the effects on bronchoalveolar lavage fluid (BALF) IL-8, neutrophils and MPO of introducing salmeterol (50 microg b.i.d.) or giving additional inhaled corticosteroid (fluticasone 100 microg b.i.d.) in 45 subjects with persistent asthma already on low/moderate doses of inhaled corticosteroids were further investigated. At baseline, BALF IL-8 but not neutrophil or MPO levels were significantly raised in the asthmatic subjects compared to normal controls. MPO levels correlated strongly with IL-8 levels, and weakly with BALF neutrophil numbers in the asthmatics. Fluticasone treatment resulted in significantly elevated neutrophil numbers, but not MPO or IL-8 levels. In contrast, introducing salmeterol significantly reduced IL-8 and MPO levels, but did not affect BALF neutrophil numbers. Interestingly, salmeterol and fluticasone showed significantly contrasting effects on MPO and neutrophils, and there was a divergent effect on IL-8 levels that almost reached significance. Excessive interleukin-8 levels may be relevant to asthma pathogenesis, even in the setting of moderate-dose inhaled corticosteroid therapy. Reduction in interleukin-8 production and possibly stabilisation of airway neutrophil numbers may explain the greater clinical benefit of adding a long-acting beta2-agonist rather than merely increasing inhaled corticosteroid doses. Indeed, high-dose inhaled corticosteroid therapy alone may promote airway neutrophilia.
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PMID:Possible anti-inflammatory effect of salmeterol against interleukin-8 and neutrophil activation in asthma in vivo. 1279 94

Perfluorocarbonic blood substitute Perftoran (PF) was used in combined intensive therapy of 79 patients with severe viral hepatitis B as a polyfunctional pathogenetic drug according to the following scheme: intravenously 400 ml 1-2 times a day for 2-6 days (800-2400 ml per course). PF exhibited immunomodulating, antioxidant, membrane-stabilizing and disintoxicating properties. The immunomodulating effect of the drug manifested itself in its influence on functional activity of macrophages, reduction of their oversection of proinflammatory cytokines: IL-1 beta, IL-6, IL-8, TNF-alpha. Antioxidant properties were established on the basis of the ability of PF to lower activity of prooxidant factors (myeloperoxidase of neutrophilic granulocytes) and to stimulate antioxidant factors (catalase, glucose-6-phosphatedehydrogenase), reduced glutathione in erythrocytes). As a membranostabilizer, PF increased resistance of erythrocyte membranes to peroxide hemolysis and improved their rheological indices (deformability and viscosity). A disintoxication effect of PF led to reduction of middle-molecular peptides content in plasma. PF had a noticeable effect on basic clinicobiochemical indices in patients with a severe course of viral hepatitis B as well as the disease course and outcomes. Finally, PF reduced the duration of treatment of patients with severe viral hepatitis B in hospital and intensive care units. It is inferred that administration of infusion drugs on the basis of perfluorocarbonic compounds holds promise in pathogenetic therapy of viral hepatitides.
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PMID:[Perfluorocarbonic compounds application as a new approach in pathogenic treatment of severe forms of viral hepatitis]. 1285 70


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