interleukin-8 has been researched along with interleukin-1beta-(163-171)* in 10 studies
1 trial(s) available for interleukin-8 and interleukin-1beta-(163-171)
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Pro- and anti-inflammatory cytokines in chronic pediatric dialysis patients: effect of aspirin.
Dialysis provides effective and safe treatment of ESRD in children, but patients who are maintained on chronic dialysis are at risk for cardiovascular disease. One major risk factor for cardiovascular disease in adult patients with ESRD is chronic inflammation. The effect of anti-inflammatory therapy with aspirin on serum cytokine concentration was studied in seven children who were receiving hemodialysis (HD) and seven who were receiving continuous cycling peritoneal dialysis (CCPD or PD). Dialysis vintage was 4.3 +/- 4.6 yr; single-pool Kt/V was 1.46 +/- 1.4, mean equilibrated Kt/V was 1.27 +/- 0.16, and PD weekly Kt/V was 2.45 +/- 0.30. Baseline proinflammatory cytokine IL-1beta, IL-6, IL-8, and TNF-alpha serum concentrations were significantly elevated, whereas serum anti-inflammatory cytokine IL-4 and IL-10 concentrations were normal. The patterns of cytokine elevation were similar for patients who were receiving HD versus PD. IL-4 and IL-6 concentrations demonstrated strong positive correlation with dialysis vintage (IL-4, P < 0.03; IL-6, P < 0.0001). Pre-aspirin serum cytokine concentrations did not vary with single-pool Kt/V or equilibrated Kt/V for HD patients or with weekly Kt/V for PD patients. Serum IL-8 and TNF-alpha concentrations were significantly reduced by aspirin treatment at 4 mo (P = 0.04 and P = 0.007, respectively). Serum IL-6 concentration decreased with aspirin treatment but not significantly (P = 0.1). Serum IL-1beta concentration remained unchanged, and IL-4 and IL-10 concentrations remained stable throughout aspirin treatment. The effect of aspirin treatment on serum cytokine concentrations was similar for HD and PD patients. In HD patients, IL-6, IL-8, and TNF-alpha remained suppressed 1 mo after discontinuation of aspirin. It is concluded that proinflammatory cytokines are elevated in pediatric HD and PD patients without counterbalance from anti-inflammatory cytokines, and aspirin therapy attenuates inflammation. Topics: Adolescent; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Child; Cytokines; Humans; Inflammation; Interleukin-10; Interleukin-1beta; Interleukin-4; Interleukin-6; Interleukin-8; Kidney Failure, Chronic; Peptide Fragments; Peritoneal Dialysis, Continuous Ambulatory; Pilot Projects; Renal Dialysis; Treatment Outcome; Tumor Necrosis Factor-alpha | 2006 |
9 other study(ies) available for interleukin-8 and interleukin-1beta-(163-171)
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Comparative Study of the Levels of IL-1β, IL-4, IL-8, TNFα, and IFNγ in Stable Course and Exacerbation of Chronic Obstructive Pulmonary Disease of Varying Severity.
In patients with chronic obstructive pulmonary disease, the levels of cytokines IL-1β, IL-4, IL-8, TNFα, and IFNγ depended on the degree of bronchial obstruction and severity and period of the disease. The maximum levels of IL-4, IL-8, and TNFα were observed in severe chronic obstructive pulmonary disease during exacerbation. The highest concentration of IL-1β and IFNγ were recorded during activation of inflammation in patients with moderate bronchial obstruction. The revealed correlations between the tested cytokines and spirometry parameters make it possible to consider the levels of these proteins as quantitative markers of systemic inflammation progression. Topics: Cytokines; Humans; Inflammation; Interferon-gamma; Interleukin-4; Interleukin-8; Pulmonary Disease, Chronic Obstructive; Tumor Necrosis Factor-alpha | 2022 |
The immune response of a warm water fish orange-spotted grouper (Epinephelus coioides) infected with a typical cold water bacterial pathogen Aeromonas salmonicida is AhR dependent.
The present study reported the first pathogenic Aeromonas salmonicida (SRW-OG1) isolated from the warm water fish orange-spotted grouper (Epinephelus coioides), and investigated the function of Aryl hydrocarbon receptor (AhR), a ligand-dependent transcriptional factor which has been recently found to be closely associated with immune response in mammals and E. coioides. Our results showed that AhR was activated by an unknown ligand in the spleen, intestine and macrophages. Meanwhile, ahr1a and ahr1b were significantly increased in the spleen, intestine and macrophages, whereas ahr2 was only increased in the intestine, which indicated that the contribution of AhR2 to the immune response may be less than that of AhR1a and AhR1b. Some key genes involved in the macrophage inflammatory response, bacterial recognition, and intestinal immunity were significantly up-regulated in the SRW-OG1 infected E. coioides. Nevertheless, declining macrophage ROS production and down-regulation of related genes were also observed, suggesting that SRW-OG1 utilized its virulence mechanisms to prevent macrophage ROS production. Furthermore, AhR inhibitor 3', 4'-DMF and the silence of ahr1a or ahr1b significantly rescued the increased IL-1β and IL-8 induced by SRW-OG1 infection, which proved that the induction of IL-1β and IL-8 in E. coioides macrophages was mediated by AhR. However, BPI/LBP, ROS production and related genes were not affected by AhR. The survival rate and immune escape rate of SRW-OG1 in the ahr1a/ahr1b knocked-down and 3', 4'-DMF treated macrophages were significantly increased compared with those in wild type macrophages. Taken together, it was preliminarily confirmed that ahr1a and ahr1b played an important role in the immune response against A. salmonicida SRW-OG1. Topics: Aeromonas salmonicida; Animals; Cell Survival; Cells, Cultured; Fishes; Gene Expression Regulation; Gene Silencing; Gram-Negative Bacterial Infections; Immune Evasion; Immunity, Innate; Interleukin-1beta; Interleukin-8; Macrophages; Organ Specificity; Peptide Fragments; Reactive Oxygen Species; Receptors, Aryl Hydrocarbon; Temperature; Virulence; Water; Zebrafish Proteins | 2020 |
Development of a biomarker mortality risk model in acute respiratory distress syndrome.
There is a compelling unmet medical need for biomarker-based models to risk-stratify patients with acute respiratory distress syndrome. Effective stratification would optimize participant selection for clinical trial enrollment by focusing on those most likely to benefit from new interventions. Our objective was to develop a prognostic, biomarker-based model for predicting mortality in adult patients with acute respiratory distress syndrome.. This is a secondary analysis using a cohort of 252 mechanically ventilated subjects with the diagnosis of acute respiratory distress syndrome. Survival to day 7 with both day 0 (first day of presentation) and day 7 sample availability was required. Blood was collected for biomarker measurements at first presentation to the intensive care unit and on the seventh day. Biomarkers included cytokine-chemokines, dual-functioning cytozymes, and vascular injury markers. Logistic regression, latent class analysis, and classification and regression tree analysis were used to identify the plasma biomarkers most predictive of 28-day ARDS mortality.. From eight biologically relevant biomarker candidates, six demonstrated an enhanced capacity to predict mortality at day 0. Latent-class analysis identified two biomarker-based phenotypes. Phenotype A exhibited significantly higher plasma levels of angiopoietin-2, macrophage migration inhibitory factor, interleukin-8, interleukin-1 receptor antagonist, interleukin-6, and extracellular nicotinamide phosphoribosyltransferase (eNAMPT) compared to phenotype B. Mortality at 28 days was significantly higher for phenotype A compared to phenotype B (32% vs 19%, p = 0.04).. An adult biomarker-based risk model reliably identifies ARDS subjects at risk of death within 28 days of hospitalization. Topics: Adult; APACHE; Biomarkers; Cytokines; Female; Humans; Interleukin 1 Receptor Antagonist Protein; Interleukin-1beta; Interleukin-6; Interleukin-8; Intramolecular Oxidoreductases; Latent Class Analysis; Logistic Models; Macrophage Migration-Inhibitory Factors; Male; Middle Aged; Nicotinamide Phosphoribosyltransferase; Peptide Fragments; Respiratory Distress Syndrome; Risk Assessment; Sphingosine-1-Phosphate Receptors; Vesicular Transport Proteins | 2019 |
Long non-coding RNA antisense non-coding RNA in the INK4 locus expression correlates with increased disease risk, severity, and inflammation of allergic rhinitis.
The aim of the current study was to investigate the expression of long non-coding RNA (lncRNA) antisense non-coding RNA in the INK4 locus (ANRIL) in allergic rhinitis (AR) patients, and to further explore the association of lncRNA ANRIL expression with AR risk, severity, and inflammation.In this case-control study, 96 AR patients and 96 non-atopic obstructive snoring patients who underwent adenoid surgery were consecutively recruited. Disease severity of AR patients was assessed via individual nasal symptom score (INSS) and total nasal symptom score (TNSS). Nasal mucosa samples were collected from AR patients and controls, then lncRNA ANRIL and inflammatory cytokine levels were assessed via quantitative polymerase chain reaction.LncRNA ANRIL expression was increased in AR patients (3.605 [1.763-4.981]) compared with controls (1.183 [0.438-2.985]), and it well distinguished AR patients from controls with an area under curve of 0.746 (95% CI: 0.679-0.814). Correlation analyses revealed that lncRNA ANRIL expression was positively associated with itching score and congestion score, while it was not associated with nasal rhinorrhea score or sneezing score. Besides, lncRNA ANRIL was also positively correlated with TNSS, tumor necrosis factor α, interleukin (IL)-4, IL-6, IL-13, and IL-17, while negatively associated with IL-10 and interferon-γ. And no association of lncRNA ANRIL expression with IL-1β, IL-5, or IL-8 expression was discovered.LncRNA ANRIL expression correlates with increased AR risk, severity, and inflammation, implying that lncRNA ANRIL might be involved in the pathogenesis of AR. Topics: Adolescent; Adult; Case-Control Studies; Cytokines; Disease Susceptibility; Female; Genetic Loci; Humans; Inflammation; Interleukin-1beta; Interleukin-5; Interleukin-8; Male; Nasal Mucosa; Peptide Fragments; Rhinitis, Allergic; RNA, Long Noncoding; Severity of Illness Index; Tumor Necrosis Factor-alpha; Young Adult | 2019 |
Cytokine induction of peripheral blood mononuclear cells by biofilms and biofilm supernatants of Granulicatella and Abiotrophia spp.
Granulicatella and Abiotrophia species are the normal oral flora bacteria that can occasionally cause infective endocarditis. Although substantial data exists in the literature demonstrating occurrence of these species in infective endocarditis, only a few mechanistic studies on their pathogenicity are found. The aim of this study was to investigate the ability of Granulicatella and Abiotrophia species to elicit immune response from human peripheral blood mononuclear cells (PBMC). Biofilms and biofilm supernatants of Granulicatella elegans CCUG 38949, Granulicatella adiacens CCUG 27809 and Abiotrophia defectiva CCUG 27639 were used to stimulate PBMCs for 24 h. Cytokines produced were first screened using a human cytokine membrane array kit. Further, pro-inflammatory cytokines TNF-α, IL-β, and IL-17 were quantified by ELISA. The cytokine profiler array showed the induction of 15 different cytokines/chemokines including IL-1β, IL-6, IL-8, TNF-α, MCP-1, MIP-1α/MIP-1β and RANTES. ELISA quantification revealed that G. adiacens biofilm induced significantly higher (P < 0.05) levels of IL-1β, i.e., 1931 (183) pg/ml than G. elegans or A. defectiva. However, in the case of biofilm supernatants A. defectiva was the strongest, inducing 2104 (574) pg/ml. Biofilm supernatants, but not biofilms from all three species induced TNF-α only weakly. IL-17 was undetectable from any of the stimulated samples. In conclusion, Granulicatella and Abiotrophia are potent inducers of inflammatory mediators from human PBMCs. However, biofilms and biofilm supernatants from these species seem to selectively elicit stimulation of certain cytokines. Topics: Abiotrophia; Arachidonic Acids; Biofilms; Carnobacteriaceae; Chemokine CCL3; Chemokine CCL4; Chemokines; Cytokines; Endocarditis, Bacterial; Humans; Interleukin-17; Interleukin-1beta; Interleukin-6; Interleukin-8; Leukocytes, Mononuclear; Peptide Fragments; Tumor Necrosis Factor-alpha | 2018 |
Astragalus polysaccharides enhance the immune response to avian infectious bronchitis virus vaccination in chickens.
Astragalus polysaccharides (APS) are biological macromolecules extracted from Astragalus species that have strong immunoregulatory properties. In this study, APS were employed as an adjuvant for an avian infectious bronchitis virus (IBV) vaccine, and its effects on the cellular immune and humoral immune responses to vaccination in chicken were investigated. One hundred and fifty chicken were randomly divided into five groups (n = 30, each group). The chickens in all groups, except for the unvaccinated control group, were vaccinated with an IBV DNA vaccine. Three of the four vaccinated groups were administered different doses of APS (APSL, 10 mg/kg; APSM, 50 mg/kg; and APSH, 100 mg/kg) after the first vaccination, and the remaining vaccinated group served as a control, without any additional treatment. At 14, 28, and 42 days after the first vaccination, serum anti-IBV antibody titers; peripheral lymphocyte proliferation; and the mRNA expression of IL-1β, IL-2, IL-8, and TNF-α in the spleen were assessed by enzyme-linked immunosorbent assay (ELISA), the cell counting kit-8 (CCK-8), and real time quantitative RT-PCR (qRT-PCR), respectively. At most time points, the titer of IBV-specific antibodies, lymphocyte proliferation, and IL-1β, IL-2, IL-8, and TNF-α mRNA expression levels were higher in three APS groups than in the vaccine control group, and these increases were dose-dependent. These data suggest that APS could be used as an adjuvant for IBV vaccination to provide better protection against IBV infection. Topics: Adaptive Immunity; Adjuvants, Immunologic; Animals; Antibodies, Viral; Astragalus Plant; Cell Proliferation; Chickens; Coronavirus Infections; Cytokines; Enzyme-Linked Immunosorbent Assay; Infectious bronchitis virus; Interleukin-1beta; Interleukin-2; Interleukin-8; Lymphocytes; Peptide Fragments; Plant Extracts; Polysaccharides; Poultry Diseases; RNA, Messenger; Spleen; Time Factors; Tumor Necrosis Factor-alpha; Vaccination; Vaccines, DNA; Viral Vaccines | 2017 |
Tocilizumab inhibits interleukin-6-mediated matrix metalloproteinase-2 and -9 secretions from human amnion cells in preterm premature rupture of membranes.
In the present study, we investigated the participation of inflammatory cytokine-induced mediated matrix metalloproteinase (MMP) expressions and inhibition of interleukin (IL)-6-induced MMP secretion in amniotic epithelial cells by tocilizumab.. To investigate the role of MMP expressions, immunohistochemical staining was performed using membranes obtained from 10 patients with preterm premature rupture of membranes (PPROM) and from 10 patients who underwent a nonlabor cesarean section. We also investigated the regulation of MMP expression by inflammatory cytokines in human amnion cells.. Immunohistochemical staining showed a significantly higher expression of MMP-2 and -9 in PPROM. Treatment of cultured WISH and primary amniotic epithelial cells with 10(-8) or 10(-7)M IL-6 or tumor necrosis factor (TNF)-alpha clearly increased the secretion of MMP-2 and -9. Treatment with 10(-8)M TNF-alpha or IL-6 significantly increased the invasion of WISH or primary amniotic epithelial cells, respectively, compared with the control. At a low concentration of 1 microg/ml, tocilizumab (anti-human IL-6 receptor monoclonal antibody) inhibited the IL-6-induced MMP secretion.. This paper is the 1st report of tocilizumab inhibiting IL-6-induced MMP-2 and MMP-9 secretions from human amnion cells in PPROM. Topics: Amnion; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Blotting, Western; Cell Line; Epithelial Cells; Female; Fetal Membranes, Premature Rupture; Humans; Immunohistochemistry; Interleukin-1beta; Interleukin-6; Interleukin-8; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; Matrix Metalloproteinase Inhibitors; Peptide Fragments; Pregnancy; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Tumor Necrosis Factor-alpha | 2009 |
[Expression of IL-8 mRNA in glomerular endothelial cells].
To study the expression of IL-8 mRNA in cultured human glomerular endothelial cells.. The effects of IL-1 beta and TNF alpha on the production of IL-8 by glomerular endothelial cells were also observed. RT-PCR was used.. There was only weak expression of IL-8 mRNA in cultured human glomerular endothelial cells without the presence of any stimulating factors, whereas the expression of IL-8 mRNA in cultured human glomerular endothelial cells was significantly increased after the glomerular endothelial cells have been treated with IL-1 beta (25 u/ml) or TNF alpha (10 ng/ml) for 24 hours.. Glomerular endothelial cell injury may enhance the expression of IL-8, which mediates the inflammatory reactions in glomeruli. Topics: Cells, Cultured; Endothelium; Gene Expression; Humans; Interleukin-1; Interleukin-1beta; Interleukin-8; Kidney Glomerulus; Peptide Fragments; Polymerase Chain Reaction; Recombinant Proteins; RNA, Messenger; Tumor Necrosis Factor-alpha | 1996 |
Cytokine, complement, and endotoxin profiles associated with the development of the adult respiratory distress syndrome after severe injury.
The adult respiratory distress syndrome (ARDS) is a frequent complication after severe accidental trauma. This study examines the hypothesis that increased systemic concentrations of proinflammatory cytokines, endotoxin, or complement fragments may predict the development of ARDS.. Prospective, observational study.. Two Level I university trauma centers.. Fifteen severely injured patients (Injury Severity Score of > or = 25).. Standard emergency department, operating room, and intensive care unit management.. Plasma samples were obtained at 4-hr intervals from the time of injury and were assayed for concentrations of endotoxin, tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, IL-8, and complement fragments C3a and C4a. Hemodynamic and oxygen metabolism variables also were measured at 4-hr intervals after injury. Seven patients developed ARDS and eight patients did not. The PaO2/FIO2 ratio was significantly decreased in the patients with ARDS compared with non-ARDS patients as early as 4 hrs postinjury, and remained significantly decreased throughout the initial 24 hrs after severe accidental injury. Plasma IL-8, IL-6, C3a, and C4a concentrations were markedly increased starting in the immediate postinjury period in both ARDS and non-ARDS patients, but no significant differences were found between the two groups until 16 hrs after injury when plasma IL-8, C3a, and C4a concentrations became significantly higher in the ARDS group. Neither the ARDS nor non-ARDS patients showed the presence of circulating IL-1 beta, TNF-alpha, or endotoxin at any postinjury time point.. These results demonstrate that measurements of plasma concentrations of proinflammatory cytokines, endotoxin, or complement fragments are not helpful in predicting the development of ARDS after severe accidental injury. Topics: Adult; Blood Gas Analysis; Complement C3a; Complement C4a; Craniocerebral Trauma; Endotoxins; Enzyme-Linked Immunosorbent Assay; Female; Hemodynamics; Humans; Injury Severity Score; Interleukin-1; Interleukin-1beta; Interleukin-6; Interleukin-8; Male; Middle Aged; Oxygen Consumption; Peptide Fragments; Predictive Value of Tests; Prognosis; Prospective Studies; Radioimmunoassay; Respiratory Distress Syndrome; Risk Factors; Survival Rate; Time Factors; Tumor Necrosis Factor-alpha | 1994 |