interleukin-8 has been researched along with Hepatitis-B* in 18 studies
1 review(s) available for interleukin-8 and Hepatitis-B
3 trial(s) available for interleukin-8 and Hepatitis-B
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Middle East Respiratory Syndrome (MERS) is a novel respiratory illness firstly reported in Saudi Arabia in 2012. It is caused by a new corona virus, called MERS corona virus (MERS-CoV). Most people who have MERS-CoV infection developed severe acute respiratory illness.. This work is done to determine the clinical characteristics and the outcome of intensive care unit (ICU) admitted patients with confirmed MERS-CoV infection.. This study included 32 laboratory confirmed MERS corona virus infected patients who were admitted into ICU. It included 20 (62.50%) males and 12 (37.50%) females. The mean age was 43.99 ± 13.03 years. Diagnosis was done by real-time reverse transcription polymerase chain reaction (rRT-PCR) test for corona virus on throat swab, sputum, tracheal aspirate, or bronchoalveolar lavage specimens. Clinical characteristics, co-morbidities and outcome were reported for all subjects.. Most MERS corona patients present with fever, cough, dyspnea, sore throat, runny nose and sputum. The presence of abdominal symptoms may indicate bad prognosis. Prolonged duration of symptoms before patients' hospitalization, prolonged duration of mechanical ventilation and hospital stay, bilateral radiological pulmonary infiltrates, and hypoxemic respiratory failure were found to be strong predictors of mortality in such patients. Also, old age, current smoking, smoking severity, presence of associated co-morbidities like obesity, diabetes mellitus, chronic heart diseases, COPD, malignancy, renal failure, renal transplantation and liver cirrhosis are associated with a poor outcome of ICU admitted MERS corona virus infected patients.. Plasma HO-1, ferritin, p21, and NQO1 were all elevated at baseline in CKD participants. Plasma HO-1 and urine NQO1 levels each inversely correlated with eGFR (. SnPP can be safely administered and, after its injection, the resulting changes in plasma HO-1, NQO1, ferritin, and p21 concentrations can provide information as to antioxidant gene responsiveness/reserves in subjects with and without kidney disease.. A Study with RBT-1, in Healthy Volunteers and Subjects with Stage 3-4 Chronic Kidney Disease, NCT0363002 and NCT03893799.. HFNC did not significantly modify work of breathing in healthy subjects. However, a significant reduction in the minute volume was achieved, capillary [Formula: see text] remaining constant, which suggests a reduction in dead-space ventilation with flows > 20 L/min. (ClinicalTrials.gov registration NCT02495675).. 3 组患者手术时间、术中显性失血量及术后 1 周血红蛋白下降量比较差异均无统计学意义(. 对于肥胖和超重的膝关节单间室骨关节炎患者,采用 UKA 术后可获满意短中期疗效,远期疗效尚需进一步随访观察。.. Decreased muscle strength was identified at both time points in patients with hEDS/HSD. The evolution of most muscle strength parameters over time did not significantly differ between groups. Future studies should focus on the effectiveness of different types of muscle training strategies in hEDS/HSD patients.. These findings support previous adverse findings of e-cigarette exposure on neurodevelopment in a mouse model and provide substantial evidence of persistent adverse behavioral and neuroimmunological consequences to adult offspring following maternal e-cigarette exposure during pregnancy. https://doi.org/10.1289/EHP6067.. This RCT directly compares a neoadjuvant chemotherapy regimen with a standard CROSS regimen in terms of overall survival for patients with locally advanced ESCC. The results of this RCT will provide an answer for the controversy regarding the survival benefits between the two treatment strategies.. NCT04138212, date of registration: October 24, 2019.. Results of current investigation indicated that milk type and post fermentation cooling patterns had a pronounced effect on antioxidant characteristics, fatty acid profile, lipid oxidation and textural characteristics of yoghurt. Buffalo milk based yoghurt had more fat, protein, higher antioxidant capacity and vitamin content. Antioxidant and sensory characteristics of T. If milk is exposed to excessive amounts of light, Vitamins B. The two concentration of ZnO nanoparticles in the ambient air produced two different outcomes. The lower concentration resulted in significant increases in Zn content of the liver while the higher concentration significantly increased Zn in the lungs (p < 0.05). Additionally, at the lower concentration, Zn content was found to be lower in brain tissue (p < 0.05). Using TEM/EDX we detected ZnO nanoparticles inside the cells in the lungs, kidney and liver. Inhaling ZnO NP at the higher concentration increased the levels of mRNA of the following genes in the lungs: Mt2 (2.56 fold), Slc30a1 (1.52 fold) and Slc30a5 (2.34 fold). At the lower ZnO nanoparticle concentration, only Slc30a7 mRNA levels in the lungs were up (1.74 fold). Thus the two air concentrations of ZnO nanoparticles produced distinct effects on the expression of the Zn-homeostasis related genes.. Until adverse health effects of ZnO nanoparticles deposited in organs such as lungs are further investigated and/or ruled out, the exposure to ZnO nanoparticles in aerosols should be avoided or minimised. Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor Proteins, Signal Transducing; Adenine; Adenocarcinoma; Adipogenesis; Administration, Cutaneous; Administration, Ophthalmic; Adolescent; Adsorption; Adult; Aeromonas hydrophila; Aerosols; Aged; Aged, 80 and over; Aging; Agriculture; Air Pollutants; Air Pollution; Airway Remodeling; Alanine Transaminase; Albuminuria; Aldehyde Dehydrogenase 1 Family; Algorithms; AlkB Homolog 2, Alpha-Ketoglutarate-Dependent Dioxygenase; Alzheimer Disease; Amino Acid Sequence; Ammonia; Ammonium Compounds; Anaerobiosis; Anesthetics, Dissociative; Anesthetics, Inhalation; Animals; Anti-Bacterial Agents; Anti-HIV Agents; Anti-Infective Agents; Anti-Inflammatory Agents; Antibiotics, Antineoplastic; Antibodies, Antineutrophil Cytoplasmic; Antibodies, Monoclonal, Humanized; Antifungal Agents; Antigens, Bacterial; Antigens, CD; Antigens, Differentiation, Myelomonocytic; Antimetabolites, Antineoplastic; Antineoplastic Agents; 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Transistors, Electronic; Translational Research, Biomedical; Transplantation Tolerance; Transplantation, Homologous; Transportation; Treatment Outcome; Tretinoin; Tuberculosis, Multidrug-Resistant; Tuberculosis, Pulmonary; Tubulin Modulators; Tumor Microenvironment; Tumor Necrosis Factor Inhibitors; Tumor Necrosis Factor-alpha; Twins; Ultrasonic Therapy; Ultrasonography; Ultraviolet Rays; United States; Up-Regulation; Uranium; Urethra; Urinary Bladder; Urodynamics; Uromodulin; Uveitis; Vasoconstrictor Agents; Ventricular Function, Left; Vero Cells; Vesicular Transport Proteins; Viral Nonstructural Proteins; Visual Acuity; Vital Capacity; Vitamin D; Vitamin D Deficiency; Vitamin K 2; Vitamins; Volatilization; Voriconazole; Waiting Lists; Waste Disposal, Fluid; Wastewater; Water Pollutants, Chemical; Whole Genome Sequencing; Wine; Wnt Signaling Pathway; Wound Healing; Wounds and Injuries; WW Domains; X-linked Nuclear Protein; X-Ray Diffraction; Xanthines; Xenograft Model Antitumor Assays; YAP-Signaling Proteins; Yogurt; Young Adult; Zebrafish; Zebrafish Proteins; Ziziphus | 2016 |
Low expression of CXCR1/2 on neutrophils predicts poor survival in patients with hepatitis B virus-related acute-on-chronic liver failure.
Polymorphonuclear neutrophils (PMNs) and proinflammatory cytokines have been implicated in the pathogenesis of acute-on-chronic liver failure (ACLF). But the utility of CXC chemokine receptor expression on PMNs as a biomarker for prediction of disease severity is still uncertain. In this study, we investigated the dynamic expression of CXCR1 and CXCR2 on neutrophils, and found that patients with hepatitis B virus-related ACLF displayed low expression of CXCR1 and CXCR2 on peripheral neutrophils compared with healthy subjects and patients with chronic hepatitis B. This expression pattern was correlated with disease severity. Additionally, increased production of IL-8 in peripheral blood was significantly associated with reduced CXCR1 and CXCR2 expression, as shown by the decreased CXCR1 and CXCR2 expression on neutrophils after treating neutrophils with plasma from ACLF patients. This effect could be overcomed through IL-8 blockage with an anti-IL-8 antibody. We also found that IL-8 production and neutrophil infiltration were coordinately increased in the liver tissue of HBV-ACLF patients, and this increase was associated with liver inflammation. Overall, increased production of IL-8 associated with neutrophils infiltration into the liver and decreased CXCR1/2 expression on peripheral neutrophils. CXCR1 and CXCR2 expression levels could be served as early markers to predict the severity of ACLF. Topics: Acute-On-Chronic Liver Failure; Adult; Biomarkers; Disease-Free Survival; Female; Gene Expression Regulation; Hepatitis B; Humans; Interleukin-8; Male; Middle Aged; Neutrophils; Receptors, Interleukin-8A; Receptors, Interleukin-8B; Survival Rate | 2016 |
Hepatitis B virus induces a novel inflammation network involving three inflammatory factors, IL-29, IL-8, and cyclooxygenase-2.
Chronic inflammation induced by hepatitis B virus (HBV) is a major causative factor associated with the development of cirrhosis and hepatocellular carcinoma. In this study, we investigated the roles of three inflammatory factors, IL-8, IL-29 (or IFN-λ1), and cyclooxygenase-2 (COX-2), in HBV infection. We showed that the expression of IL-29, IL-8, and COX-2 genes was enhanced in HBV-infected patients or in HBV-expressing cells. In HBV-transfected human lymphocytes and hepatocytes, IL-29 activates the production of IL-8, which in turn enhances the expression of COX-2. In addition, COX-2 decreases the production of IL-8, which in turn attenuates the expression of IL-29. Thus, we proposed that HBV infection induces a novel inflammation cytokine network involving three inflammatory factors that regulate each other in the order IL-29/IL-8/COX-2, which involves positive regulation and negative feedback. In addition, we also demonstrated that COX-2 expression activated by IL-8 was mediated through CREB and C/EBP, which maintains the inflammatory environment associated with HBV infection. Finally, we showed that the ERK and the JNK signaling pathways were cooperatively involved in the regulation of COX-2. We also demonstrated that IL-29 inhibits HBV replication and that IL-8 attenuates the expression of IL-10R2 and the anti-HBV activity of IL-29, which favors the establishment of persistent viral infection. These new findings provide insights for our understanding of the mechanism by which inflammatory factors regulate each other in response to HBV infection. Topics: Adult; Carcinoma, Hepatocellular; Cell Line, Tumor; Cyclooxygenase 2; Feedback, Physiological; Female; Hep G2 Cells; Hepatitis B; Hepatitis B virus; Hepatocytes; Humans; Inflammation; Inflammation Mediators; Interferons; Interleukin-8; Interleukins; Liver Neoplasms; Lymphocytes; Male; Middle Aged; Transfection; Up-Regulation | 2011 |
15 other study(ies) available for interleukin-8 and Hepatitis-B
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Interleukin-8 predicts short-term mortality in acute-on-chronic liver failure patients with hepatitis B-related-related cirrhosis background.
Acute-on-chronic liver failure (ACLF) is a distinctive and severe syndrome, marked by an excessive systemic inflammatory response. In vivo, interleukin 8 (IL-8) is an essential pro-inflammatory cytokine. We aimed to investigate the value of serum IL-8 levels in predicting mortality in ACLF patients in the background of hepatitis B virus-related cirrhosis.. In this study, we conducted a retrospective analysis of the clinical baseline characteristics of 276 patients with ACLF in the context of HBV-related cirrhosis. Logistic regression analysis was employed to identify independent risk factors for short-, intermediate-, and long-term mortality. Using these independent risk factors, we developed a nomogram model, which was subsequently validated. To assess the clinical usefulness of the nomogram model, we performed decision curve analysis (DCA).. Out of the 276 patients with ACLF, 98 (35.5%), 113 (40.9%), and 128 (46.4%) died within 28, 90, and 180 days, respectively. Serum IL-8 levels were only an independent predictor of 28-day mortality and could simply classify ACLF patients. Conversely, mean arterial pressure (MAP), HBV-DNA, and COSHACLF IIs were independent predictors of mortality across all three observation periods. We constructed a nomogram based on IL-8 that was able to visualise and predict 28-day mortality with a C-index of 0.901 (95% CI: 0.862-0.940). Our calibration curves, Predicted Probability of Death & Actual Survival Status plot, and Confusion Matrix demonstrated the nomogram model's strong predictive power. DCA indicated the nomogram's promising clinical utility in predicting 28-day mortality in ACLF patients.. Serum IL-8 levels predict short-term mortality in ACLF patients in the background of HBV-associated cirrhosis, and the developed Nomogram model has strong predictive power and good clinical utility.. Systemic inflammatory response is a pathophysiological feature of patients with acute-on-chronic liver failure, and the serum level of interleukin-8 can predict the short-term prognosis of patients. Topics: Acute-On-Chronic Liver Failure; Hepatitis B; Hepatitis B, Chronic; Humans; Interleukin-8; Liver Cirrhosis; Prognosis; Retrospective Studies | 2023 |
Hepatitis B-Induced IL8 Promotes Hepatocellular Carcinoma Venous Metastasis and Intrahepatic Treg Accumulation.
Hepatitis B-associated hepatocellular carcinoma (HCC) is often accompanied by severe vascular invasion and portal vein tumor thrombus, leading to a poor prognosis. However, the underlying mechanism of this disease remains obscure. In this study, we demonstrate that the hepatitis B virus (HBV)-encoded gene HBx induces high IL8 production through MEK-ERK signal activation, leading to enhanced endothelial permeability to facilitate tumor vascular invasion. In a vascular metastatic model using a tail vein injection in a transgenic mouse with selective expression of human CXCR1 in the endothelium, activation of the IL8-CXCR1 cascade by overexpression of IL8 in tumor cells dramatically enhanced liver metastasis. Mechanistically, IL8 selectively induced GARP-latent-TGFβ in liver sinusoidal endothelial cells and subsequently provoked preferential regulatory T-cell polarization to suppress antitumor immunity. Collectively, these findings reveal a hepatitis B-associated IL8-CXCR1 signaling axis that mediates vascular invasion and local microenvironmental immune escape of HCC to induce intrahepatic metastasis, which may serve as potential therapeutic targets for HBV-associated HCC. SIGNIFICANCE: This study identifies a hepatitis B-induced IL8/CXCR1/TGFβ signaling cascade that suppresses antitumor immunity and enhances metastasis in hepatocellular carcinoma, providing new potential targets for therapeutic intervention. Topics: Animals; Carcinoma, Hepatocellular; Disease Models, Animal; HEK293 Cells; Hep G2 Cells; Hepatitis B; Hepatitis B virus; Human Umbilical Vein Endothelial Cells; Humans; Interleukin-8; Liver; Liver Neoplasms; MAP Kinase Signaling System; Mice; Mice, Inbred C57BL; Mice, Transgenic; Receptors, Interleukin-8A; Recombinant Proteins; T-Lymphocytes, Regulatory; Trans-Activators; Transfection; Viral Regulatory and Accessory Proteins | 2021 |
Hepatitis B vaccine non response: A predictor of latent autoimmunity?
Unresponsiveness to Hepatitis B virus (HBV) vaccine has been associated with interleukins involved with Th1 functioning including Interleukin-8 (IL-18) and Interferon-γ (IFN-γ). IL-18 and IFN-γ have also been implicated in the onset of different types of immune-mediate inflammatory conditions such as Type 1 Diabetes (T1D), Celiac disease (CD), rheumatoid arthritis (RA), obesity and systemic lupus erythematosus (SLE). Taking into account that HBV vaccination is provided in the 1st year of life worldwide, I propose that all babies should be tested for anti-HBs response after completion of the vaccine series. And I suggest that children with undetectable anti-HBs titers after recommended immunization schedule as well as the additional booster doses should be followed up over time because they may be at risk of developing a number of autoimmune disorders. In this light, the non-responsiveness to HBV vaccine might be a predictor of latent autoimmunity. For that reason, research studies are needed in order to verify the existence of potential IL-18 and IFN-γ gene polymorphisms to utilize as biomarkers of latent autoimmunity. As a final point, administration of neutralizing antibodies against IFN-γ and/or IL-18 might represent a future target for immune-modulatory therapeutic approach to halt or even reverse autoimmune phenomena. Topics: Autoimmunity; Diabetes Mellitus, Type 1; Hepatitis B; Hepatitis B Antibodies; Hepatitis B Vaccines; Humans; Inflammation; Interferon-gamma; Interleukin-18; Interleukin-8; Models, Theoretical; Polymorphism, Genetic; Treatment Outcome | 2017 |
Comparative Analysis of Liver Injury-Associated Cytokines in Acute Hepatitis A and B.
Acute hepatitis A (AHA) and acute hepatitis B (AHB) are caused by an acute infection of the hepatitis A virus and the hepatitis B virus, respectively. In both AHA and AHB, liver injury is known to be mediated by immune cells and cytokines. In this study, we measured serum levels of various cytokines and T-cell cytotoxic proteins in patients with AHA or AHB to identify liver injury-associated cytokines.. Forty-six patients with AHA, 16 patients with AHB, and 14 healthy adults were enrolled in the study. Serum levels of 17 cytokines and T-cell cytotoxic proteins were measured by enzyme-linked immunosorbent assays or cytometric bead arrays and analyzed for correlation with serum alanine aminotransferase (ALT) levels.. Interleukin (IL)-18, IL-8, CXCL9, and CXCL10 were significantly elevated in both AHA and AHB. IL-6, IL-22, granzyme B, and soluble Fas ligand (sFasL) were elevated in AHA but not in AHB. In both AHA and AHB, the serum level of CXCL10 significantly correlated with the peak ALT level. Additionally, the serum level of granzyme B in AHA and the serum level of sFasL in AHB correlated with the peak ALT level.. We identified cytokines and T-cell cytotoxic proteins associated with liver injury in AHA and AHB. These findings deepen the existing understanding of immunological mechanisms responsible for liver injury in acute viral hepatitis. Topics: Acute Disease; Adult; Alanine Transaminase; Biomarkers; Cytokines; Enzyme-Linked Immunosorbent Assay; Fas Ligand Protein; Female; Hepatitis A; Hepatitis A virus; Hepatitis B; Hepatitis B virus; Humans; Interleukin-22; Interleukin-6; Interleukin-8; Interleukins; Liver Failure; Male; Middle Aged; T-Lymphocytes, Cytotoxic | 2016 |
HBV/HCV dual infection impacts viral load, antibody response, and cytokine expression differently from HBV or HCV single infection.
Hepatitis B virus/hepatitis C virus (HBV/HCV) dual infection is common among high-risk individuals. To characterize the virological and immunological features of patients with HBV/HCV dual infection, we enrolled 1,049 individuals who have been identified as injection drug users. Patients were divided into single and dual infection groups according to the serological markers. We found the average HCV RNA level was significantly lower; however, HBV viral load was significantly higher in HBV/HCV dual-infected patients (n = 42) comparing HCV single infection (n = 340) or HBV single infection (n = 136). The level of anti-HBs in patients who experienced spontaneous HBV clearance was higher than that in HCV single-infected patients with HBV spontaneous clearance. The level of anti-HCV E2 in HBV/HCV dual infection was lower than that detected in HCV single infection. Serum levels of IL-6, IL-8, and TNF-α were significantly lower in HBV/HCV dual-infected patients than in patients infected with HBV or HCV alone. Taken together, two viral replications are imbalanced in dual infected patients. The anti-HBs and anti-HCV E2 antibody production were impaired and proinflammatory IL-6, IL-8, and TNF-α also downregulated due to dual infection. These findings will help further understanding the pathogenesis of HBV/HCV dual infection. Topics: Adult; Antibody Formation; Cytokines; Female; Hepacivirus; Hepatitis B; Hepatitis B virus; Hepatitis C; Humans; Interleukin-6; Interleukin-8; Male; RNA, Viral; Serologic Tests; Tumor Necrosis Factor-alpha; Viral Load; Virus Replication | 2016 |
[Clinical and immunological features of acute hepatitis B in patients with concomitant chronic toxic liver damage].
The article presents information obtained during the survey in 64 patients with acute hepatitis B. We show that acute hepatitis B in patients with concomitant chronic toxic liver characterized by a marked imbalance of cytokine status due to a lower level of interleukin-2 and a higher content of interleukin-8, the highest levels of nitrite content, spontaneous oxidative modifications of blood proteins and the lowest content of L -arginine in the blood serum in the dynamics of disease compared with patients without this concomitant factor. In the period of convalescence these changes in patients with acute hepatitis B with concomitant chronic toxic liver characterized combined with higher cytolysis of liver cells, often circulating in the blood of HBsAg seroconversion and less frequently with the advent of anti-HBeAg. Topics: Adolescent; Aged; Aged, 80 and over; Blood Proteins; Female; Hepatitis B; Hepatitis B Antibodies; Hepatitis B e Antigens; Hepatitis B Surface Antigens; Hepatitis B virus; Humans; Interleukin-2; Interleukin-8; Liver; Male; Middle Aged; Phylogeny | 2013 |
Downregulation of the AU-rich RNA-binding protein ZFP36 in chronic HBV patients: implications for anti-inflammatory therapy.
Inflammation caused by chronic hepatitis B virus (HBV) infection is associated with the development of cirrhosis and hepatocellular carcinoma; however, the mechanisms by which HBV infection induces inflammation and inflammatory cytokine production remain largely unknown. We analyzed the gene expression patterns of lymphocytes from chronic HBV-infected patients and found that the expression of ZFP36, an AU-rich element (ARE)-binding protein, was dramatically reduced in CD4(+) and CD8(+) T lymphocytes from chronic HBV patients. ZFP36 expression was also reduced in CD14(+) monocytes and in total PBMCs from chronic HBV patients. To investigate the functional consequences of reduced ZFP36 expression, we knocked down ZFP36 in PBMCs from healthy donors using siRNA. siRNA-mediated silencing of ZFP36 resulted in dramatically increased expression of multiple inflammatory cytokines, most of which were also increased in the plasma of chronic HBV patients. Furthermore, we found that IL-8 and RANTES induced ZFP36 downregulation, and this effect was mediated through protein kinase C. Importantly, we found that HBsAg stimulated PBMCs to express IL-8 and RANTES, resulting in decreased ZFP36 expression. Our results suggest that an inflammatory feedback loop involving HBsAg, ZFP36, and inflammatory cytokines may play a critical role in the pathogenesis of chronic HBV and further indicate that ZFP36 may be an important target for anti-inflammatory therapy during chronic HBV infection. Topics: Adult; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Chemokine CCL5; China; Cytokines; DNA Primers; Female; Gene Expression Regulation; Gene Knockdown Techniques; Hepatitis B; Hepatitis B Surface Antigens; Humans; Inflammation; Interleukin-8; Leukocytes, Mononuclear; Male; Middle Aged; Real-Time Polymerase Chain Reaction; RNA, Small Interfering; Tristetraprolin | 2012 |
Licensing virus-specific T cells to secrete the neutrophil attracting chemokine CXCL-8 during hepatitis B virus infection.
T cell functional plasticity helps tailor antiviral immunity during different phases of infections. We tested whether, during different phases of HBV infection, virus-specific T cells can acquire specific proinflammatory functions that could drive granulocyte/mononuclear cell liver infiltration. Multifunctional analysis of HBV-specific T cells during acute and chronic HBV infection revealed that HBV-specific T cells had the capacity to produce the neutrophil chemokine CXCL-8 but not IL-17. CXCL-8 producing T cells were detectable in the liver of chronic HBV patients with active hepatitis; while in acute HBV patients CXCL-8 production by T cells was temporally limited to the acute phase of disease, concomitant with the peak of liver inflammation. Characterization of the conditions necessary for the development of CXCL-8 producing T cells showed a requirement for IL-7 and IL-15 during T cell expansion. These data show that functional plasticity of virus-specific T cells spontaneously occurs during HBV infection and that an environment rich IL-7 and IL-15 can license T cells with the ability to produce CXCL-8 and potentially influence liver pathology. Topics: Acute Disease; CD8-Positive T-Lymphocytes; Cells, Cultured; Chemokines; Hepatitis B; Hepatitis B virus; Humans; Interleukin-15; Interleukin-17; Interleukin-8; Liver; Neutrophils; Peptides; Species Specificity; T-Lymphocytes; Viral Proteins | 2011 |
Correlation between hyporesponsiveness to Toll-like receptor ligands and liver dysfunction in patients with chronic hepatitis C virus infection.
Hepatitis C virus (HCV)-associated antigens, such as the core and nonstructural antigens, activate host innate immune systems via Toll-like receptors (TLRs). We previously showed that chronic exposure to the core antigen induces hyporesponsiveness to TLR ligands in antigen-presenting cells via activation of TLR2 and that stimulation with TLR ligands results in impaired IL-6 production by peripheral blood monocytes from HCV-infected patients. In the present study, peripheral blood mononuclear cells (PBMCs) isolated from patients with chronic HCV or hepatitis B virus (HBV) infection were stimulated with TLR ligands to determine the production of IL-6 and IL-8 and to identify the clinical parameters associated with hyporesponsiveness to TLR ligands in patients with chronic HCV infection. The results showed that pro-inflammatory cytokine responses to TLR ligands were suppressed in PBMCs isolated from HCV-infected, but not HBV-infected, patients. The reduced cytokine responses to TLR ligands seen in HCV-infected patients correlated with platelet counts and serum prothrombin time levels. In contrast, there was no correlation between TLR-induced cytokine responses and serum levels of core antigen. Thus, hyporesponsiveness to TLR ligands in HCV-infected patients is correlated with liver dysfunction. In conclusion, both host factors and viral factors may be involved in the generation of hyporesponsiveness to TLR ligands in patients with chronic HCV infection. Topics: Adult; Aged; Antigens, Viral; Female; Hepacivirus; Hepatitis B; Hepatitis C, Chronic; Humans; Interleukin-6; Interleukin-8; Leukocytes, Mononuclear; Liver Diseases; Male; Middle Aged; Platelet Count; Prothrombin Time; Toll-Like Receptors | 2011 |
Characterization of interleukin 8 in woodchucks with chronic hepatitis B and hepatocellular carcinoma.
The eastern woodchuck, Marmota monax, represents a useful animal model to study hepatitis B virus infection in humans. However, immunological studies in this model have been impeded by a lack of basic information about the components of the immune system such as cytokines and chemokines. To clarify the role(s) of interleukin 8 (IL-8) in chronic hepatitis B and hepatocellular carcinoma (HCC) in the woodchuck model, we cloned and characterized the woodchuck IL-8 cDNA and genomic DNA. Sequence analysis revealed that the organization of the wk-IL-8 gene is similar to that of the human IL-8 gene and consists of four exons and three introns. Woodchuck IL-8 protein exhibits the conserved ELRCXC motif of IL-8 and shows 87, 82, 82 and 79% similarity with rabbit, ovine, bovine and human IL-8 proteins, respectively. The biological activity of wk-IL-8 was demonstrated using neutrophil chemotaxis assays. Wk-IL-8 could be readily detected in both tumor and non-tumor tissues with higher expression in the non-tumor tissues in most cases. The results from this study will facilitate the investigation of IL-8 in the immunopathogenesis of hepadnavirus-related diseases by the woodchuck model. Topics: Amino Acid Motifs; Amino Acid Sequence; Animals; Base Sequence; Carcinoma, Hepatocellular; Cell Line; Cells, Cultured; Conserved Sequence; Disease Models, Animal; DNA, Complementary; DNA, Viral; Exons; Hepatitis B; Hepatitis B Virus, Woodchuck; Hepatitis, Viral, Animal; Humans; Interleukin-8; Introns; Kidney; Liver Neoplasms, Experimental; Marmota; Molecular Sequence Data; Sequence Homology, Amino Acid; Viral Load | 2009 |
[Clinical laboratory and morphologic characteristic of mixed hepatitis B + C with manifestation of its course].
Topics: Hepatitis B; Hepatitis C; Humans; Interleukin-1; Interleukin-2; Interleukin-8; Lymphocytes; Military Personnel; Russia | 2002 |
[The transcription and expression of IL-18 gene in HBV infectors].
To evaluate the possible roles of interleukin 18 (IL-18) in hepatitis B virus (HBV) infection.. Peripheral blood lymphocytes from 3 groups of HBV infectors (including 15 asymptomatic carriers, 30 patients with chronic hepatitis, 12 patients with fulminant hepatitis) and 10 blood donors (as normal controls) were analyzed. The transcription and expression of IL-18 in PBMC were assessed by semi-quantitive reverse transcription polymerase chain reaction and flow cytometry.. (1) There were significant differences in the transcription and expression levels of IL-18 between each group of HBV infectors. Interestingly, it was highest in fulminant hepatitis group, and lowest in asymptomatic carrier group. However there was no significant difference between chronic hepatitis and normal controls. The severity of disease was accompanied with the elevation of IL-18 production. (2) The severity degree of liver inflammation in chronic hepatitis was ccompanied with the elevation of IL-18 production. (3) The transcription and expression of IL-18 in chronic hepatitis B correlated with serum ALT positively (r = 0.54, P < 0.01; r = 0.63, P < 0.01). (4) There was a positive correlation in transcription and expression of IL-18 in each group of HBV infectors (asymptomatic carrier r = 0.980, P < 0.001; chronic hepatitis r = 0.910, P < 0.001; fulminant hepatitis r = 0.975, P < 0.001).. IL-18 may take part in the host immunity against HBV,and relate to the inflammation degree of liver. Topics: Female; Gene Expression; Hepatitis; Hepatitis B; Hepatitis B virus; Humans; Immunity; Interleukin-8; Male; RNA, Messenger | 2001 |
Plasma interleukin-8 levels in patients with post-hepatitic cirrhosis: relationship to severity of liver disease, portal hypertension and hyperdynamic circulation.
The present study investigated plasma levels of interleukin-8 (IL-8) in patients with post-hepatitic cirrhosis and correlated it with the severity of liver diseases and haemodynamic parameters. Plasma IL-8 levels were significantly higher in 57 post-hepatitic cirrhotic patients (7.5 +/- 1.8 pg/mL; P < 0.005) than those in 41 healthy subjects (2.0 +/- 0.2 pg/mL). Elevated (> 5 pg/mL) plasma IL-8 levels were found in up to 30% of cirrhotic patients. In cirrhotic patients, plasma IL-8 levels progressively increased in relation to the severity of liver dysfunction (4.5 +/- 1.0, 4.9 +/- 1.4 and 20.5 +/- 8.3 pg/mL for Pugh's class A, B and C, respectively; P < 0.005). A significant correlation was observed between plasma IL-8 levels and serum bilirubin levels (r = 0.72; P < 0.001). There were no differences in the hepatic venous pressure gradient (15.4 +/- 1.1 vs 15.1 +/- 0.9 mmHg; P > 0.05) and systemic vascular resistance (1119 +/- 118 vs 1199 +/- 54 dyn.s/cm5; P > 0.05) between cirrhotic patients with and without elevated plasma IL-8 levels. In addition, plasma IL-8 levels did not correlate with hepatic venous pressure gradient (r = 0.26; P > 0.05) and systemic vascular resistance (r = -0.24; P > 0.05). These results demonstrate that plasma IL-8 levels are increased in patients with post-hepatitic cirrhosis. The severity of liver cirrhosis is an important factor for the occurrence of enhanced IL-8 levels. IL-8 does not play a role in the hyperdynamic circulation observed in patients with post-hepatitic cirrhosis. Topics: Bilirubin; Female; Hepatitis B; Hepatitis C; Humans; Hypertension, Portal; Interleukin-8; Liver; Liver Circulation; Liver Cirrhosis; Male; Middle Aged; Vascular Resistance; Venous Pressure | 1996 |
Interleukin-8 and granulocyte-macrophage colony-stimulating factor secretion in hepatocellular carcinoma and viral chronic active hepatitis.
Interleukin-8 (IL-8) and granulocyte-macrophage colony-stimulating factor (GM-CSF) are important mediators of inflammation and immune response in human disease. To demonstrate their importance in pathophysiological processes in liver disease, we measured the circulating levels of IL-8 and GM-CSF in patients with hepatocellular carcinoma (HCC) and chronic active hepatitis (CAH). IL-8 and GM-CSF levels in serum samples were determined with highly specific and sensitive enzyme-linked immunosorbent assays. IL-8 levels were more elevated in serum samples of patients with HCC and CAH associated with hepatitis C virus infection than HCC and CAH associated with hepatitis B virus infection. However, in all patients with autoimmune CAH and in some patients with HCC and CAH, GM-CSF levels were elevated over the baseline levels measured in all of the normals, but this difference was not statistically significant for any group. We conclude that IL-8 and GM-CSF are increased in some patients with liver diseases, and as such they may play a significant role in host defense and disease. Topics: Carcinoma, Hepatocellular; Female; Granulocyte-Macrophage Colony-Stimulating Factor; Hepatitis B; Hepatitis C; Hepatitis, Chronic; Humans; Interleukin-8; Liver Neoplasms; Male; Middle Aged; Reference Values | 1995 |
IL-8 as a circulating cytokine: induction by recombinant tumour necrosis factor-alpha.
Tumour necrosis factor-alpha (TNF-alpha) is a pivotal cytokine at the centre of a cascade of cytokines and inflammatory mediators which modulate the host response to infection and trauma, and in particular the metabolic changes resulting in shock and subsequent multi-organ failure. The cytokine IL-8--predominantly an activator and chemotactic factor for circulating polymorphonuclear neutrophil leucocytes--is produced in response to TNF-alpha in vitro, and high circulating levels of IL-8 are found in septic primates. We have studied the release of IL-8 into the circulation of subjects with chronic hepatitis B undergoing a 10 week pilot trial of recombinant TNF-alpha (rTNF-alpha) therapy in doses of 15-100 micrograms/m2. A marked dose-dependent increase in plasma IL-8 levels was seen commencing at 30-60 min after the start of rTNF-alpha infusion and peaking between 2 and 3 h (mean peak level 4300 ng/l). The temporal pattern of IL-8 production exactly echoed that of IL-6, another component of the cytokine cascade, but peak plasma levels of IL-8 were up to 17 times higher than those of IL-6. This study confirms in vitro data suggesting that IL-8 is a component of the acute circulating cytokine cascade with a potential role in the modulation of the acute immune and metabolic response to infection and trauma. Topics: Chronic Disease; Dose-Response Relationship, Drug; Enzyme-Linked Immunosorbent Assay; Hepatitis B; Humans; Infusions, Intravenous; Interleukin-6; Interleukin-8; Pilot Projects; Time Factors; Tumor Necrosis Factor-alpha | 1992 |