UNIPROT:P10145 - FACTA Search

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Query: UNIPROT:P10145 (IL-8)
23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review focuses on bacterial induction and release of inflammatory cytokines and adhesion molecules by human bronchial epithelial cells, with special reference to Haemophilus influenzae, a pathogen commonly associated with chronic bronchitis. Studies investigating the mechanisms underlying bacterial colonization of the airways and bacterial-induced chronic airway inflammation have suggested that these are likely to involve localization of bacteria to the site(s) of infection in the respiratory tract and induction of a local airway inflammation resulting in the initiation of epithelial damage. We have hypothesized that the gross airway epithelial damage observed in chronic infective lung disease is an indirect consequence of proteolytic enzymes and toxic oxygen radicals generated by large numbers of neutrophils infiltrating the airways. Furthermore, the infiltration and activation of the neutrophils is a consequence of increased release of proinflammatory mediators from the host respiratory epithelium, induced by bacterial products, such as endotoxin. This hypothesis is based on studies which have demonstrated that the concentrations of circulating cytokines, such as interleukin (IL)-8 and tumour necrosis factor-alpha (TNF-alpha), which have profound effects on neutrophil activity, are increased in endotoxaemia and that airway epithelial cells are a rich source of these cytokines. Support for this hypothesis is provided by studies of cultured human bronchial epithelial cells incubated either in the absence or presence of purified endotoxin preparations from nontypable and type b H. influenzae strains which have demonstrated that these endotoxins lead to significantly increased expression and/or release of proinflammatory mediators, including IL-6, IL-8, TNF-alpha and intercellular adhesion molecule-1 (ICAM-1). Treatment of the cells with steroids can downregulate the expression and/or release of these inflammatory mediators. Additionally, these studies have demonstrated that culture medium collected from endotoxin-treated cultures, 24 h after treatment, significantly increases neutrophil chemotaxis and adhesion to human endothelial cells in vitro.
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PMID:Bacterial-induced release of inflammatory mediators by bronchial epithelial cells. 888 Jan 12

Humans exhibit an acute inflammatory response in the lungs after controlled laboratory exposure to ozone. The present study was designed to test whether biomarkers of inflammation are detectable in humans exposed to ozone and associated copollutants under natural conditions outdoors. Bronchoscopy with bronchoalveolar lavage (BAL) was carried out on 19 normal volunteer joggers from Governors Island, NY, who exercised in the afternoon during the 1992 summer (S1) season. Fifteen subjects were retested during the following, low ozone, winter season (W). The BAL protocol involved an initial instillation of 20 ml saline followed by four sequential 50-ml saline washes carried out in both the right middle lobe and the lingula. The eight 50-ml samples were pooled as the 'alveolar' sample. Analyses performed on the alveolar lavage samples included cell differentials, release of IL-8, TNF-alpha, and reactive oxygen species (ROS) by pooled cells, and levels of IL-8, protein, LDH, fibronectin, alpha1-antitrypsin (alpha1-AT), complement fragment 3a (C3a), and prostaglandin E2 (PGE2) in lavage fluids. Release of ROS by stimulated BAL cells was lower in S1 than in W (p = 0.03). In contrast, LDH levels in BAL fluids were 2-fold higher in S1 than in W (p = 0.02), as were IL-8 (p = 0.12) and PGE2 (p = 0.06). These results suggest a possible ongoing inflammatory response in the lungs of recreational joggers exposed to ozone and associated copollutants during the summer months.
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PMID:Biomarkers of lung inflammation in recreational joggers exposed to ozone. 891 60

Multiple organ dysfunction syndrome (MODS) is a critical condition developing in the patients under overwhelming surgical insults such as a major surgery, severe trauma, extensive burn, and systemic sepsis. The host response to those surgical insults is the main pathogenetic factor contributing to the development of shock and MODS seen in surgical patients. The proinflammatory cytokines, TNF-alpha (TNF) and interleukin-1 beta (IL-1), are known to play a pivotal role in the pathogenetic mechanisms of MODS. In response to surgical insults, macrophages produce and release TNF and IL-1 which subsequently induce the production of other cytokines (IL-6, IL-8, etc.) and other endogenous chemical mediators (growth factors, adhesion molecules, complement cleavage products, thrombin, eicosanoids, PAF, nitric oxides, oxygen-free radicals, granulocyte elastase, etc.) The resultant systemic inflammation may develop into shock and MODS when the primary insults are overwhelming (early MODS) or a second inflammatory insult such as sepsis triggers an exaggerated inflammation. In the patients suffering from MODS, a systemic release of various cytokines is not properly regulated, and the high blood levels of the proinflammatory cytokines induce an autodestructive generalized inflammatory reaction. This condition is termed "Cytokine Storm" by the author. In the cytokine storm, not only proinflammatory cytokines but also anti-inflammatory cytokines are elevated in the blood stream. With the recent understanding of the biological and pathological roles of cytokines and other mediators, a new therapeutic strategy has been developed. In addition to the reduction of the surgical insults, a variety of anti-cytokine therapy and anti-mediator therapy has been tested in an attempt to prevent or treat the life-threatening MODS.
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PMID:[Cytokine storm in the pathogenesis of multiple organ dysfunction syndrome associated with surgical insults]. 894 Jun 90

In order to elucidate the role of interleukin 8 (IL-8) on the development of chronic lung disease (CLD) in neonates following an episode of respiratory distress syndrome (RDS), serial and simultaneous measurements of the concentration of IL-8 and granulocyte elastase alpha 1 proteinase inhibitor complex (E-alpha 1 PI) in the tracheobronchial aspirate of very low birthweight infants with RDS were conducted. The concentration of IL-8 and E-alpha 1 PI in infants with CLD was low in the first 48 h of life, but dramatically increased after 48 h. The concentration of IL-8 between 48 h of life and day 5 was significantly correlated to the fraction of inspired oxygen concentration (FiO2) within 48 h of age, but not to the mean airway pressure. Interleukin 8 seemed to stimulate neutrophils to release granulocyte elastase which, in turn, caused lung tissue injury, resulting in the development of CLD. It is suggested that high FiO2 is an important factor causing IL-8 production in the lung.
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PMID:Interleukin 8 and granulocyte elastase alpha 1 proteinase inhibitor complex in the tracheobronchial aspirate of infants with chronic lung disease following respiratory distress syndrome. 894 99

The kinetics of IL-8, tumour necrosis factor-alpha (TNF-alpha) and IL-1 beta release by PMN adhered to fibronectin, laminin or plastic for 24 h in response to continuous stimulation with lipopolysaccharide (LPS; 50 ng/ml), N-formyl-Met-Leu-Phe (fMLP; 100 mM), or phorbol myristate acetate (PMA; 10 ng/ml), was investigated under altered oxygen tension conditions. Cell supernatants were sampled for cytokine content every 6 h and measured by ELISA. IL-8 was the most abundant cytokine, produced in a range of up to 5.4 ng/ml; TNF-alpha and IL-1 beta were produced in a range of up to 1 ng/ml. During normoxia, LPS was the most potent stimulus, inducing the release of each cytokine, while fMLP showed a less pronounced effect on IL-8 and IL-1 beta production and markedly inhibited TNF-alpha production. PMA markedly suppressed IL-8 and IL-1 beta release and failed to induce any release of TNF-alpha. Hypoxia had an overall inhibitory effect on cytokine release except for PMA-induced IL-1 beta release, and hypoxia/reoxygenation had a significant up-regulating effect except for a further inhibition of fMLP-induced release of TNF-alpha. Integrinmatrix protein ligation differentiated both spontaneous and externally induced cytokine release and its sensitivity to alteration in oxygen tension. Thus the process of PMN elaboration of inflammatory cytokines is controlled on multiple levels of signal transduction, differentiated by integrin-extracellular matrix interactions, and is sensitive to alterations in microenvironmental oxygen tension.
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PMID:Polymorphonuclear leucocyte (PMN)-derived inflammatory cytokines--regulation by oxygen tension and extracellular matrix. 897 28

The presence of various cytokines, namely hepatocyte growth factor (HGF), interleukin-1 receptor antagonist (IL-1 RA), and interleukins (IL-1 alpha, IL-6, and IL-8), as well as the production of reactive oxygen species (ROS) was investigated in seminal plasma of fertile and infertile patients in order to evaluate the possible value of measuring these substances for the diagnosis of male accessory gland infection, and to assess the possible relationship between oxidative stress and cytokines during leucocytospermia and male accessory gland infection (MAGI). Our findings indicate that all of the measured cytokines seem to be produced locally as well as by white blood cells (WBC) and that, due to the presence of higher numbers of WBC, accessory gland infection may exert a deleterious effect on sperm quality through the production of ROS and/or of particular cytokines such as IL-1 alpha, IL-1 RA, and IL-8. The most specific marker for a sensitivity of 95% in discriminating between cases with or without MAGI is the measurement of IL-6 in seminal plasma. In the absence of WBC several cytokines are constitutively produced and correlate with sperm concentration (HGF, IL-8), alpha-glucosidase (IL-6), and gamma-glutamyltransferase activity (HGF). The measurement of these cytokines in semen may provide clinically useful information for the diagnosis of male accessory gland infection, as well as in the absence of WBC where it can provide information about certain mechanisms of male reproductive function and dysfunction.
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PMID:The relation between reactive oxygen species and cytokines in andrological patients with or without male accessory gland infection. 901 1

In response to a variety of stimuli, e.g. pathogens, phagocytes release reactive oxygen species which are essential for bacterial killing and also potentiate inflammatory reactions. We have used flow cytometry measurements to study the priming process of phagocyte oxidative burst in whole blood, in order to avoid introducing artefacts due to the purification process and to stimulate the in vivo situation more closely. In these conditions, we examined the in vitro effects of proinflammatory cytokines (TNF-alpha, IL-1 alpha, IL-1 beta, IL-6, IL-8 and GM-CSF) on the PMN oxidative burst. We found that none of the cytokine tested directly activated the PMN oxidative burst. In contrast, TNF, GM-CSF and IL-8 strongly primed a subpopulation of PMN which produced large amounts of H2O2 in response to fMLP, suggesting that these cytokines may play a critical role in bactericidal killing in vivo. Furthermore, we reported a decreased H2O2 production by TNF or IL-8 primed PMN in HIV-infected patients. This impairment, which correlated with the clinical stage of the disease, could contribute to the increased susceptibility to bacterial infections in HIV-infected patients. In addition, we reported the case of a child with severe recurrent infections due to intracellular microorganisms which could be related to an impairment of the phagocyte priming process of the oxidative burst [corrected].
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PMID:Priming study of human phagocytes oxidative burst by using flow cytometry. 903 Sep 65

1. Helicobacter pylori infection is characterized by an infiltration of neutrophils in the gastric mucosa. Neutrophil activation is an important source of reactive oxygen radicals, which cause tissue damage. Studies have shown that in Helicobacter pylori-infected patients there is increased mucosal production of interleukin 8. However, the role of interleukin 8 in the Helicobacter pylori-related inflammatory process and its relationship with reactive oxygen radicals remains to be clarified. The aims of this study were to investigate if there is any association between antral mucosal levels of interleukin 8 and reactive oxygen radicals and their relationship to gastric antral inflammation. 2. Fifty-two patients referred for endoscopy were recruited into the study. Gastric antral biopsies were taken for histology, culture and measurement of interleukin 8 and chemiluminescence (measuring reactive oxygen radicals). Interleukin 8 was measured by ELISA and the result expressed as pg/mg biopsy. Luminol-enhanced chemiluminescence was measured as mV min-1 mg-1 biopsy. Antral inflammation was assessed by a pathologist in a blinded fashion. 3. Antral mucosal levels of interleukin 8 and reactive oxygen radicals were significantly higher in Helicobacter pylori-colonized mucosa than in Helicobacter pylori-negative mucosa. After the eradication of Helicobacter pylori in patients with duodenal ulcer the median values (ranges) of interleukin 8 and reactive oxygen radicals fell from 1.21 (0.10-2.40) to 0.65 (0.00-1.60) and from 110.0 (10.0-959.0) to 14.5 (0.0-85.0) respectively. There was a positive correlation between interleukin 8 concentration and chemiluminescence response in the antral mucosa (r = 0.72). A higher interleukin 8 concentration was associated with greater neutrophil infiltration (r = 0.72) and mononuclear cell infiltration (r = 0.55); the magnitude of the chemiluminescence response was also positively associated with neutrophil (r = 0.77) and mononuclear cell infiltration (r = 0.59). 4. Interleukin 8 concentration is associated with an infiltration of neutrophils and mononuclear cells and is correlated with the production of reactive oxygen radicals in antral gastric mucosa infected with Helicobacter pylori. These findings suggest that interleukin 8 may be important in attracting and activating phagocytes to release reactive oxygen radicals, thereby causing mucosal damage.
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PMID:Association of antral mucosal levels of interleukin 8 and reactive oxygen radicals in patients infected with Helicobacter pylori. 903 94

We investigated the hypothesis that CD54 (intercellular adhesion molecule-1) expressed on hepatocytes will support beta2-integrin (CD18)-dependent adhesion of neutrophils. An in vitro model using C3A cells (a human hepatoblastoma cell line exhibiting many characteristics of normal hepatocytes) and human neutrophils was utilized. C3A cells were stimulated with interleukin-1beta (IL-1beta), tumor necrosis factor-alpha, or interferon-gamma (IFN-gamma) for 24 h to induce expression of CD54, and adhesion of neutrophils was found to be markedly increased. Detailed studies with IFN-gamma-stimulated (100 U/ml) C3A cells revealed that this adhesion involved CD11a/CD18 [lymphocyte function-associated antigen-1 (LFA-1)] and CD54 and was dependent on low levels of IL-8 produced by the stimulated hepatocytes. Addition of higher concentrations of chemotactic factor (e.g., IL-8) further augmented adhesion and recruited contributions of CD11b/CD18 (Mac-1). In contrast to LFA-1, Mac-1 appeared to recognize a CD54-independent ligand constitutively expressed on the hepatocytes. Such close apposition of neutrophils to hepatocytes may increase the potential for parenchymal cell injury by providing a short distance through which cytotoxic factors such as reactive oxygen or proteolytic enzymes could act.
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PMID:CD18 integrin and CD54-dependent neutrophil adhesion to cytokine-stimulated human hepatocytes. 912 60

Infectious complications are the leading cause of death in acute pancreatitis. Individual factors of immune defence could be of significance, whether or not a patient develops a severe course with infectious complications. In a prospective 5-year trial including 72 patients, we investigated 29 cellular and humoral markers of the body's defence system for their potential to indicate the severity and course of acute pancreatitis. Complement factors C3 and C4 as well as immunoglobulins IgG, IgM and IgA were normal, in general. Measurable levels of IL-1 alpha, IL-1 beta, IL-2 and sIL-2R could be detected only occasionally. Values of alpha 1-AT, TNF-alpha, TNF alpha-Rp75, neopterin, sICAM-1, IL-8, IL-1RA and sIL-6R did not correlate with a severe course. Due to the high magnitude of increase, CRP, IL-6 and granulocyte elastase were the best indicators of the inflammatory process. Delayed-type hypersensitivity response was the only early predictor of a severe course. It was superior over other cellular markers such as monocyte count or CD4+/CD8+ ratio. In vitro function of polymorphonuclear granulocytes (PMN) was not adequate to the severity of the disease already during the first week of illness. During further course, PMN motility and capacities to produce reactive oxygen species even worsened. The compromized PMN function could explain the frequent development of infectious complications in patients suffering from severe pancreatitis. These results should encourage new concepts of infection prophylaxis using stimulants of cellular defence.
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PMID:[Cellular and humoral functions in acute pancreatitis]. 913

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