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)

Respiratory virus are the most frequent cause of asthma attacks, and are responsible for more than 80% of episodes of wheezing in children. Atopic subjects have a higher risk of respiratory virus infections, benign or severe, than healthy persons. In children older than 8 years, most respiratory infections are caused by rhinovirus (RV). RV colonizes the respiratory epithelium and provokes a symptomatic rhinitis by non-inflammatory routes (with non involvement of leucocytes). In the nose the most importance of these routes are nerves. In the lower respiratory airways, infection with RV causes an inflammatory reaction with persistence of eosinophils. IL-8 and the other cytokines produced by the infected epithelium extend the action of eosinophils and the inflammatory reaction. The viral/inflammatory pathway is an important new target for development of strategies for the prevention of asthma.
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PMID:[Respiratory inflammation]. 922 Oct 15

A crossover trial was conducted to evaluate the acute human health effects of a dust control technology in a swine confinement facility. Twenty lifetime nonsmoking male subjects, with no evidence of allergy or asthma and no previous swine barn exposure, participated in the study, which included a laboratory session (baseline), 5-h exposure in a swine room sprinkled with canola oil (treatment) and 5-h exposure in a traditional swine room (control). Mean values of inhalable dust concentrations and endotoxin levels in the control room were significantly greater than those observed in the treatment room. Mean shift changes in FEV1 from preexposure to end of exposure were 1.1% (standard error, 0.63%) on baseline day, -1.9% (0.63%) on treatment day, and -9.9% (1.12%) on control day; the differences in the shift changes were statistically significant. Mean value of methacholine concentration that reduced the FEV1 by 20% (PC20) in bronchoprovocation tests on baseline day was significantly different from that on treatment day (p = 0.04) and that on control day (p < 0.001). Significant increases were also observed in white blood cell counts and nasal lavage cell counts on the control day in comparison with the other two days. Blood neutrophil counts after control room exposure were twice those observed on baseline and after exposure to the treatment room. Significant differences were also observed in IL-1 beta, IL-6, and IL-8 nasal lavage cytokines and in IL-6 serum cytokine. These results suggest that the canola oil dust control method is effective in improving indoor air quality in swine barns and reducing acute health effects in naive healthy subjects.
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PMID:Positive human health effects of dust suppression with canola oil in swine barns. 927 17

Asthma exacerbations are often associated with respiratory virus infections, particularly with rhinovirus. In the present study we investigated the effect of experimental rhinovirus 16 (RV16) infection on airway inflammation as assessed by analysis of hypertonic saline-induced sputum. Twenty-seven nonsmoking atopic, mildly asthmatic subjects participated in a placebo-controlled parallel study. RV16 (n = 19) or its diluent (n = 8) was nasally administered. Sputum inductions were performed at entry and on Days 2 and 9 after inoculation, and airway responsiveness to histamine (PC20) was measured on Days 4 and 11. Cell differentials and levels of albumin, eosinophil cationic protein (ECP), IL-8, and IL-6 were determined. The cellular origin of IL-8 was investigated by intracellular staining. RV infection was confirmed by culture and/or by antibody titer rise in each of the RV16-treated subjects. There were no significant changes in the sputum differentials of nonsquamous cells (MANOVA, p > or = 0.40). In the RV16 group, there was a significant increase in the levels of ECP, IL-8, and IL-6 at Day 2 after infection (p < 0.05), whereas the albumin levels did not change (p = 0.82). The levels of IL-8 and IL-6 remained elevated for as long as 9 d after infection (p < 0.05). The increase in the percentage of IL-8 positive cells at Day 2 after infection could be attributed to the increase in IL-8 positive neutrophils (p < 0.02). There was a significant decrease in PC20 at Day 4 (p = 0.02), which was no longer significant at Day 11 (p = 0.19). The decrease in PC20 correlated significantly with the increase in ECP in the first week (r = -0.60) and with the change in the percentage eosinophils in the second week after inoculation (r = -0.58). We conclude that experimental RV16 infection in atopic asthmatic subjects increases airway hyperresponsiveness in conjunction with augmented airway inflammation, as reflected by an increase in ECP, IL-8, and IL-6 in sputum. Our results suggest that the RV16-enhanced airway hyperresponsiveness is associated with eosinophilic inflammation.
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PMID:Experimental rhinovirus 16 infection. Effects on cell differentials and soluble markers in sputum in asthmatic subjects. 927 47

Airway inflammation is a very important feature of asthma and occurs simultaneously with increased hyperreactivity. We have examined whether the local inflammation provoked by histamine and allergen challenge of patients with atopic bronchial asthma is associated with the appearance, in vivo interleukin-B (IL-8) in bronchoalveolar lavage fluid (BAL). Bronchoscopy and BAL for further IL-8 investigation were performed before and 24 h after challenge test with histamine (n = 11), grass pollen antigen (n = 8) and PBS (n = 5). ELISA test was used to measure IL-8 concentration (pg/ml) (kits from R&D, USA). There was observed increased level of IL-8 (p < 0.05) after histamine and allergen challenge test. This increased level of IL-8 was correlated with neutrophils in BAL (Kendall's correlation coefficient = +0.5). We conclude that IL-8 may participate in creation of bronchial hyperreactivity in atopic bronchial asthma.
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PMID:[The effect of bronchial inhalation provocation tests on levels of interleukin-8 in material from broncho-alveolar fluid of patients with atopic bronchial asthma]. 929 96

The airway epithelial cell may play a role as an effector cell, releasing various cytokines and extracellular matrix components in immune responses, inflammation, and wound repair processes, thus contributing to cytokine "networks." The cytokines transforming growth factor (TGF)-beta and interleukin (IL)-4 are though to have pivotal roles in airway diseases, with IL-4 having proinflammatory actions and TGF-beta generally regarded to mediate repair and to attenuate immune responses. In asthma, where IL-4 and TGF-beta are thought to contribute to the inflammatory process and repair, respectively, interactions between these cytokines are likely to be of importance. Therefore, we studied the potential interaction of both cytokines by measuring IL-8 and fibronectin release by cultured human bronchial epithelial cells (HBECs). IL-4 is capable of inducing IL-8 release from HBECs. This effect of IL-4 can be blocked by the concurrent presence of the cytokine TGF-beta. In contrast, TGF-beta had a modest inconsistent stimulatory effect on IL-8 release by itself and had no effect on the IL-8 release induced by tumor necrosis factor (TNF)-alpha. An antagonistic effect of IL-4 and TGF-beta was also observed on HBEC fibronectin release. TGF-beta stimulated fibronectin release, and IL-4 was able to inhibit this. This effect was not due to a redistribution of fibronectin but appeared to be due to a true reduction in synthesis. Consistent with this, IL-4 and TGF-beta effects on IL-8 and fibronectin release were paralleled by changes in mRNA levels. The ability of TGF-beta to block IL-4-induced IL-8 release is certainly not the only mechanism to inhibit IL-8 release because dexamethasone was capable of inhibiting both TNF-alpha- and IL-4-induced release of IL-8. These results indicate that TGF-beta and IL-4 can have mutually inhibitory effects. The balance determined by this reciprocal inhibition may play an important role in regulating inflammation repair and in diseases such as asthma.
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PMID:Mutual inhibition by TGF-beta and IL-4 in cultured human bronchial epithelial cells. 931 7

The present consensus on the diagnosis and treatment of asthma relies on symptoms and lung function measurements for the monitoring of disease severity. Even though this probably remains the cornerstone of asthma management, the rapidly increasing insight into the pathogenesis and pathophysiology of the disease is presently leading to the development of more direct measurements of airway inflammation, which may provide potentially relevant information on its clinical course and prognosis. However, at present none of these has sufficiently been validated for current use in monitoring patients with asthma. First, there are new ways of looking at symptoms and lung function. Careful measurements of symptoms by visual analogue scale (VAS) are suggesting that inflammatory activity within the airways can be subjectively perceived, a sensitivity which may be blunted in patients with brittle asthma. In addition, modern physiological parameters, such as the degree of bronchodilatation following a deep breath (M/P-ratio), are strongly associated with airway inflammation. Second, there are multiple cellular and/or soluble markers of inflammation in peripheral blood (using PCR, in situ hybridization, flow cytometry, or circulating mediators and cytokines) and in urine (LTE4, EPX). Recently this has been extended by similar measurements in hypertonic saline-induced sputum (cell differentials and specific stainings on cytospins, flow cytometry, and levels of e.g. ECP, IL-5, IL-8). Finally, mediators and cytokines in the condensate of exhaled air (H2O2, leukotrienes, IL-5?) as well as exhaled NO are currently under evaluation. Adding such markers of airway inflammation as guides in asthma therapy is potentially useful. As a first step towards such a new approach we have recently shown that adding the reduction of airway hyperresponsiveness to the aims of asthma therapy leads to a better clinical as well as histological outcome after two years of treatment. In conclusion, there are new and exciting perspectives in the monitoring of disease severity in asthma in the future. Longitudinal studies presently ongoing will elucidate which parameter is potentially most useful in guiding asthma management.
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PMID:Non-invasive monitoring of bronchial inflammation in asthma. 935 60

Exacerbations of asthma are often associated with respiratory infection caused by rhinoviruses. To study the effects of rhinovirus infection on respiratory epithelium, a primary target for respiratory viruses, human rhinovirus (HRV)-2 and HRV-14 were infected to primary cultures of human tracheal epithelial cells. Viral infection was confirmed by showing that viral titers of supernatants and lysates from infected cells increased with time and by polymerase chain reaction. HRV-2 and HRV-14 infections upregulated the expression of intercellular adhesion molecule-1 (ICAM-1) mRNA, the major rhinovirus receptor, on epithelial cells, and they increased the production of interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor (TNF)-alpha in supernatants. Antibodies to ICAM-1 inhibited HRV-14 infection of epithelial cells and decreased the production of cytokines after HRV-14 infection, but they did not alter HRV-2 infection-induced production ofcytokines. IL-1beta upregulated ICAM-1 mRNA expression and increased susceptibility to HRV-14 infection, whereas other cytokines failed to alter ICAM-1 mRNA expression. Furthermore, a neutralizing antibody to IL-1beta significantly decreased viral titers of supernatants and ICAM-1 mRNA expression after HRV-14 infection, but a neutralizing antibody to TNF-alpha was without effect. Immunohistochemical studies revealed that both HRV-14 infection and IL-1beta increased ICAM-1 expression on cultured epithelial cells. These findings imply that HRV-14 infection upregulated ICAM-1 expression on epithelial cells through increased production of IL-1beta, thereby increasing susceptibility to infection. These events may be important for amplification of airway inflammation after viral infection in asthma.
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PMID:Rhinovirus infection of primary cultures of human tracheal epithelium: role of ICAM-1 and IL-1beta. 935 49

Chemotaxis of guinea pig eosinophils induced by various stimuli in use of a modified Boyden chamber technique in vitro and the effect of a platelet-activating factor (PAF) antagonist, apafant (CAS 105219-56-5, WEB 2086 BS), on it were examined. The eosinophils were obtained by bronchoalveolar lavage from the animals treated by i.v. injection with Sephadex G-200 and purified by Percoll density gradient centrifugation. PAF significantly and potently induced the chemotaxis at a broad range of 10(-17) to 10(-7) mol/l, where no concentration-dependency was observed. Leukotriene B4 also induced the chemotaxis in a concentration-dependent manner at 10(-14) to 10(-12) mol/l and the enhanced migration was not declined until 10(-7) mol/l. Interleukin-5 (IL-5), IL-8 and regulated on activation normal T expressed and secreted (RANTES) only modestly enhanced the chemotaxis in some concentrations at 10(-13) to 10(-7) mol/l with or without significance and with no concentration-dependency while formyl-methionyl-leucyl-phenylalanine (FMLP), a known chemoattractant, increased the migration at 10(-7) to 10(-5) mol/l. Apafant at 10(-8) to 10(-6) mol/l strongly and concentration-dependently inhibited 10(-8) mol/l PAF-induced chemotaxis. However, the drug showed nominal or no influences on their chemotaxis stimulated by the other agonists, at the concentrations of which the enhanced migration was observed. From these results, it is concluded that IL-5, IL-8 and RANTES, different from PAF and LTB4, are not potent stimuli for the eosinophil chemotaxis and that apafant is a selective antagonist of PAF, which is expected to be therapeutically effective for PAF-associated diseases including bronchial asthma.
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PMID:Eosinophil chemotaxis induced by several biologically active substances and the effects of apafant on it in vitro. 936 4

An imbalance of proinflammatory cytokines such as TNF-alpha, IL-1 beta, and the neutrophil chemotactic factor IL-8 and inhibitors (e.g., soluble TNF receptors and IL-1ra) in the lung during the first week of life may contribute to prolonged pulmonary inflammation and fibrosis in bronchopulmonary dysplasia (BPD). Disodium cromoglycate (DSCG) has anti-inflammatory effects in asthma, a disease with many similarities with BPD. In a prospective, randomized, blinded study, we examined whether early DSCG therapy inhibits proinflammatory cytokines in infants at risk for BPD. Twenty-six infants who were identified as high risk (> or = 75% probability) for oxygen-dependency at 28 d by a 12-h predictive score and survived 48 h were randomized to nebulized DSCG 20 mg (n = 13) or 2 cc NS (control, n = 13) every 6 h from Day 3 to Day 28. Lung lavage was collected on Day 3 (pre-study) and Day 7 and analyzed for cell count and differential and TNF-alpha, sTNFR1, sTNFR2, IL-1 beta, IL-1ra, and IL-8 concentrations. The groups' pre-study lavage cytokine concentrations were similar, but TNF-alpha and IL-8 concentrations were 3.6- and 4.9-fold lower in the DSCG group on Day 7 compared with levels in the control group. Soluble TNF receptors were unaffected by DSCG. There was a trend towards lower IL-1 beta levels in DSCG-treated infants on Day 7, but IL-1ra levels were unaffected by DSCG therapy. Three control subjects, but no DSCG-treated infants, died during the study period (p = 0.07). There were no significant differences between survivors of the two groups for oxygen-dependency at 28 d (100% control subjects; 85% DSCG). These results suggest that nebulized DSCG may exert an anti-inflammatory effect in the lungs of infants < or = 1,000 g at risk for BPD.
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PMID:Cromolyn sodium prophylaxis inhibits pulmonary proinflammatory cytokines in infants at high risk for bronchopulmonary dysplasia. 937 70

To provide bases of comparison between the studies described in Parts I and II of this Research Report, concentrations of interleukin 6 (IL-6)*, interleukin 8 (IL-8), and alpha 2-macroglobulin (a2M) were measured in airway lavage fluids obtained in the Balmes study (Part I) and compared with the same measurements in the Frampton study (Part II). For healthy subjects in the Balmes study, IL-6 and a2M, but not IL-8, increased in association with ozone exposure. Statistical analyses suggested that effects of ozone on IL-8 levels observed in the first exposure and bronchoscopy may have carried over to the second exposure and bronchoscopy, which may have obscured an effect of ozone on IL-8 after the second exposure. For asthmatic subjects in the Balmes study, IL-6 and IL-8 increased in both bronchial and alveolar lavage fluid, but not in proximal airway lavage fluid. The mean interval between exposures was longer for asthmatic subjects than for healthy subjects, and no carryover effects were seen. When the Balmes and Frampton data were analyzed together, subject groups in the two studies (nonsmokers, smokers, and subjects without and with asthma) did not differ significantly in the response of cytokines to ozone exposure. The finding of possible carryover effects in one group suggests that subtle effects of ozone exposure, or bronchoscopy including proximal airway lavage and biopsy, or both, may persist for three weeks in some subjects.
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PMID:Effects of ozone on normal and potentially sensitive human subjects. Part III: Mediators of inflammation in bronchoalveolar lavage fluid from nonsmokers, smokers, and asthmatic subjects exposed to ozone: a collaborative study. 938 97


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