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)

Beta 2-receptor agonists have recently been reported to be effective on allergen-induced late-phase reaction (LPR) in addition to their inhibitory effect on immediate-phase reaction, although the precise mechanism is not fully understood. In this study, we tested the effect of a selective beta 2-agonist, procaterol, on human basophil migration, which may be an important characteristic of LPR. Procaterol inhibited IL-8- and C5a-induced basophil migration in a dose-dependent fashion; 10(-7) M of procaterol reduced 30% of migration induced by both factors. The action of procaterol was rapid since the inhibition of migration was detected without preincubation and was not via the toxic effect on basophils as assessed by trypan blue test. The results of this study extend the repertoire of anti-inflammatory actions of beta 2-agonists.
J Asthma 1995
PMID:A beta 2-agonist, procaterol, inhibits basophil migration. 755 62

Asthma and chronic obstructive pulmonary disease are characterized by chronic airway inflammation. Studies using bronchoalveolar lavage (BAL) have shown an increased proportion of eosinophils in the BAL fluid from asthmatics compared with that from normal subjects, whereas studies of chronic obstructive pulmonary disease (COPD) have shown increased numbers of neutrophils. Induced sputum allows sampling of respiratory tract secretions from patients and control subjects, providing a noninvasive method of studying airway secretions and allowing characterization of cells and measurement of soluble markers. We investigated whether induced sputum was a useful method of studying airway fluid from patients with moderate to severe COPD and whether it could be used to compare inflammation in this condition with that in asthma. An initial reproducibility study was undertaken. Sputum was induced twice in 13 patients with severe COPD at a 14-d interval. Total and differential cell counts were carried out and were found to be reproducible over this period. Sputum was then induced in 14 patients with COPD, 23 patients with asthma, 12 healthy cigarette smokers, and 16 normal nonsmoking control subjects. We found a significant increase in neutrophils and increased concentrations of tumor necrosis factor-alpha (TNF alpha) and interleukin-8 (IL-8) in the patients with COPD compared with the smoking and nonsmoking control subjects. Interleukin-8, but not TNF alpha, was significantly higher in the COPD group than in the asthmatic group. We conclude that the cytokines TNF alpha and IL-8 may be involved in the inflammation in COPD.
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PMID:Differences in interleukin-8 and tumor necrosis factor-alpha in induced sputum from patients with chronic obstructive pulmonary disease or asthma. 856 92

Nasal provocation (NP) in allergic rhinitis patients can elicit a late phase inflammatory response in which interleukins (IL), leukotrienes (LT), and neutrophils have been implicated. Certain antihistamines have been shown to have anti-inflammatory properties. The objective was to determine whether astemizole at 10 mgs/day has any anti-inflammatory characteristics. We clinically evaluated 20 patients with allergic rhinitis and measured nasal IL-8 and LTB4 during NP with increasing doses of grass and ragweed antigen in a double-blind placebo-controlled fashion after a 4-week course of treatment. Clinical symptom scores for sneezing, pruritus, and rhinorrhea were evaluated. Nasal fluid was examined by ELISA and RIA for IL-8 and LTB4 levels along with neutrophil assessment before NP and at 3, 6, and 8 hours. Symptom scores for nasal sneezing, pruritus, rhinorrhea, and nasal LTB4 levels at 6 and 8 hours and IL-8 at 3, 6, and 8 hours were generally lower in astemizole-treated patients compared to those on placebo. Nasal IL-8 levels corresponded to LTB4 levels at diluent and at 6 hours in the placebo group (P = 0.01). The percentage of neutrophils correlated with LTB4 levels at baseline, coefficient = 0.76, P = 0.02 and at 6 hours, coefficient = 0.62, P = 0.035 in the placebo group. This study is the first to demonstrate an effect of astemizole during NP on IL-8 and LTB4 levels with a significant correlation of neutrophil numbers in untreated patients during the nasal late phase response.
Allergy Asthma Proc
PMID:Late phase response during nasal challenge: effect of astemizole on leukotriene B4 levels. 893 1

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

Asthma is an inflammatory disease of the airways, and exacerbations of this disease have been associated with high levels of air pollution. The objective of this study was to examine whether ambient air pollution and/or allergen exposure induces inflammatory changes in the upper airways of asthmatics. Sixty patients with intermittent to severe persistent asthma visited the Hospital's Out Patient Clinic every 2 wk for a period of 3 mo, and on each visit a nasal lavage was obtained. Associations between nasal inflammatory parameters and seasonal allergens and/or air pollution exposures were analyzed using linear regression analysis. The study ran from July 3 to October 6, 1995, during which period ozone (8-h mean: 80 micrograms/m3) and PM10 (24-h mean: 40 micrograms/m3) were the major air pollutants; the major aeroallergen was mugwort pollen (24-h mean: 27 pollen grains/m3). Effects on both cellular and soluble markers in nasal lavage were demonstrated for both ozone and mugwort pollen, but not for PM10. Ambient ozone exposure was associated with an increase in neutrophils (112% per 100 micrograms/m3 increase in 8-h average ozone concentration), eosinophils (176%), epithelial cells (55%), IL-8 (22%), and eosinophil cationic protein (ECP) (19%). Increases in environmental mugwort pollen counts were associated with an increase in nasal eosinophils (107% per 100 pollen/m3) and ECP (23%), but not with neutrophils, epithelial cells, or lL-8. This study demonstrated that both ambient ozone and allergen exposure are associated with inflammatory responses in the upper airways of subjects with asthma, although the type of inflammation is qualitatively different.
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PMID:Effects of photochemical air pollution and allergen exposure on upper respiratory tract inflammation in asthmatics. 941 53

Asthma is considered a Th2-like disease, characterized by locally increased levels of interleukin (IL) 4. The bronchial epithelium plays an important role in the initiation and perpetuation of inflammatory reactions within the airways. However, little is known about the presence of IL-4 receptors on human bronchial epithelial cells, or the effects of IL-4 on these cells. In this report, definitive evidence of IL-4 receptor expression on human bronchial epithelial cells using several methods is presented. IL-4 receptor expression on human bronchial epithelial cells in vivo was demonstrated using in situ hybridization and immunohistochemistry. No difference in IL-4 receptor protein expression was observed between bronchial biopsies of healthy subjects compared to allergic asthmatics. Cultured human bronchial epithelial cells also expressed IL-4 receptor mRNA and protein (as determined by RT-PCR analysis and flow cytometry, respectively). IL-4 receptor protein expression by bronchial epithelial cells could be increased by stimulation with PMA+calcium ionophore, whereas IL-1beta and IL-6 decreased IL-4 receptor expression. A cyclic AMP analogue and IL-4 had no effect. Finally, it is shown that the IL-4 receptor is functionally active as IL-4 stimulates the release of IL-8, monocyte chemoattractant protein 1, and particularly IL-1 receptor antagonist by human bronchial epithelial cells. It is concluded that human bronchial epithelial cells express IL-4 receptors both in vivo and in vitro. Stimulation of human bronchial epithelial cells by IL-4 may result in the release of both pro- and anti-inflammatory mediators known to be upregulated in asthmatic airways.
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PMID:Interleukin 4 receptors on human bronchial epithelial cells. An in vivo and in vitro analysis of expression and function. 981 35

Asthma is a chronic inflammatory lung disease in which eosinophils are one of the most important involved cells. These cells accumulate in the lung because of cytokines, which are able to regulate cellular responses. The role of cytokines is well known in allergic asthma: IL4, IL5, IL3, GMCSF are the principally cytokine involved. IL4 regulate IgE synthesis while IL5, (and IL3) cause the activation and accumulation of eosinophils. In non allergic asthma, whilst only IL5 seemed to be important recent data, shows that also IL4 plays an important role. Therefore nowadays no relevant difference seems to exist between allergic and non allergic asthma; instead the primer is different: the allergen in allergic asthma and often an unknown factor in the non allergic asthma. Recently other cytokines have been proved to play a role in the pathogenesis of asthma. IL8 is chemotactic not only for neutrophils but also for eosinophils and might cause chronic inflammation in severe asthma. IL13 works like IL4, while RANTES seems to be a more important chemotactic agent than IL5. Finally IL10, which immunoregulates T lymphocyte responses, may reduce asthma inflammation. In conclusion cytokine made us to learn more about the pathogenesis of asthma even if we do not yet know when and how asthma inflammation develops.
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PMID:[Cytokines and asthma]. 984 56

In recent years there has been an explosive expansion of knowledge relating to a family of proteins involved in the intercellular communication network of the immune system. These substances, referred to as cytokines, are importantly involved in the highly regulated complex sequence of events of cellular interaction that comprise immune responses. Atopic diseases, which afflict 20-30% of the general population, are now considered to be associated with a set of abnormal genetically regulated immune responses to foreign antigens, i.e., allergens. The atopic individuals is characterized by the excessive production of IgE antibody to allergens after inhalation, ingestion, and surface contact. There are now recognized over 19 major classes of cytokines, which have been organized into the following categories according to their major functional activities: 1) Acute phase reactants, promoting and mediating natural immunity (e.g., IL-1, IL-6, TNF, interferons alpha and beta, and IL-8); 2) Cytokines that mediate cellular growth and differentiation (e.g., IL-7, IL-4, IL-2, IL-5, IL-10, IL-12, IL-13); 3) Cytokines that act as hematopoietic growth factors (IL-3, GMCSF, IL-9, IL-11, stem cell factor); 4) Chemokines (alpha and beta major groups, DTG, RANTES); and 5) Cytokines that exert lymphocyte regulatory activity (EG, IFN-gamma, TGF). Of particular importance to allergic disease is the recent recognition of the regulation of helper immune function by two lineages of T helper cells, i.e., Th1 and Th2, by these cytokines. The Th2 hypothesis of allergy (4) considers atopy as a Th2-driven hypersensitivity reaction to allergens of complex genetic and environmental origins, in which the Th1 lineage, normally driven by IL-2, TNF, and IFN-gamma is deficient, and in which a predominant Th2 response is seen that is driven by IL-4, IL-13, IL-5, and IL-10. This knowledge is finding application in both the diagnosis and therapy of allergic diseases, through the measurement or use of cytokines, which may replace deficient quantities, or the use of anticytokines, which may neutralize elevated quantities of cytokines, events that collectively contribute to the immunologic imbalance characteristic of the allergic state. In the future, the application of cytokines will continue to find clinical application in allergic disease, and it behooves the clinical allergist-immunologist to keep abreast of the exciting new developments that are occurring in this field.
Allergy Asthma Proc
PMID:Cytokines and allergic diseases: clinical aspects. 987 71

Cytokines as soluble proteins or growth factors involved in cellular interactions are major contributors to allergic and immune-mediated inflammation. Chemokines are chemoattractive cytokines subdivided into families based on cysteine residues. This review on corticosteroid effects on cytokines and chemokines will consider only a selected number of several of these proteins studied in our division and in other centers. Characteristics of several major cytokines up to IL-15, chemokine targets and the effect of corticosteroids on various cells, cytokines, and chemokines are reviewed. The effect of corticosteroid inhibitors of non-specific endothelial activation, selective activation of VCAM-1 expression, eosinophil priming and chemokine production related to allergic diseases is illustrated. The effect of nasal corticosteroids on IL-1 beta, RANTES, IL-6, and IL-8 is also discussed.
Allergy Asthma Proc
PMID:Corticosteroid effects on cytokines and chemokines. 1038 47

Airway inflammation in severe asthma is not well characterized but may involve neutrophils. We have compared induced sputum profiles in patients with asthma of varying severity and normal control subjects. We have also measured exhaled nitric oxide (NO) as a noninvasive marker of inflammation. Asthma severity was based on clinical features before treatment and the minimum medication required to maintain asthma control at the time of sputum induction, and classified as (1) mild: treated with inhaled beta(2)-agonist occasionally (n = 23; FEV(1), 91%; peak expiratory flow (PEF) variability, 10.5%), (2) moderate: requiring medium dose inhaled steroids to maintain control (n = 16; FEV(1), 88%; PEF variability, 9.1%), and (3) severe: despite using inhaled and oral steroids (n = 16; FEV(1), 61%; PEF variability, 36.2%). The asthmatic patients were nonsmokers with evidence of airway hyperresponsiveness or reversible airway obstruction, and free of respiratory tract infection for at least 6 wk. Sputum revealed significantly increased neutrophil numbers in severe asthma (53.0 [38.4- 73.5]%, p < 0.05) compared with mild asthma (35.4 [29.8-46.1]%) and normal control subjects (27.7 [20.6-42.2]%). Interleukin-8 (IL-8) and neutrophil myeloperoxidase (MPO) levels were increased in asthmatic patients, with the highest levels in severe asthma. Eosinophil numbers were increased in both mild and severe asthma, but interleukin-5 (IL-5) levels were highest in mild asthma, whereas eosinophil cationic protein (ECP) levels were highest in severe asthma. Exhaled NO levels were highest in asthmatic untreated with corticosteroids, but there was no significant difference between asthmatics using corticosteroids (Groups 2 and 3), regardless of clinical asthma severity. This confirms the role of eosinophils in asthma but suggests a potential role of neutrophils in more severe asthma.
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PMID:Neutrophilic inflammation in severe persistent asthma. 1055 16


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