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)

We have previously reported that TNF alpha's ability to induce neutrophil transendothelial and transepithelial migration was largely dependent on the generation of IL-8 by the endothelial or pulmonary epithelial cells. To further explore the interrelationship of IL-8 with TNF alpha, we examined the migration of human neutrophils through noncellular barriers in response to these cytokines alone or in combination. We directly compared neutrophil migration through 3 microns-pore size polycarbonate Transwell filters in response to 10 nM TNF alpha or either 10 nM TNF alpha or buffer plus 10(-8) to 10(-11) M IL-8. We found that the combination of TNF alpha and IL-8 induced neutrophil migration that was generally additive, and sometimes synergistic, to that of either agent alone. In conclusion, these data support the role of cytokine networking in inducing neutrophil-rich lung inflammatory responses.
Allergy Asthma Proc
PMID:Combination of IL-8 plus TNF alpha induces additive neutrophil migration. 1062 91

Cytokine-mediated interactions among the inflammatory cells may play a role in the pathogenesis of bronchial asthma. Interleukin-8 (IL-8) is a major cytokine in the recruitment of neutrophils to the area of inflammation. Serum IL-8 is a marker of disease activity and treatment efficacy in bronchial asthma. To understand the role of IL-8 in disease activity in acute asthma, changes in serum concentrations of IL-8 elaborated by activated eosinophil before and after prednisolone therapy with clinical improvement were determined in the present study. Circulating levels of IL-8 in 15 normal control subjects and in sera from 20 allergic asthmatic children with acute exacerbation and in stable condition were determined by using commercially available assay kits. The mean concentration of serum IL-8 was statistically significantly higher in asthmatic children with acute exacerbation (63.62 +/- 11.41 pg/mL) and in stable asthmatics (64.22 +/- 10.31 pg/mL) compared to the control group subjects (50.40 +/- 30.70 pg/mL; p < 0.01). However, the difference was not statistically significant between the acute exacerbation and stable asthmatics groups (p > 0.05). Serum IL-8 is a poor indicator of disease activity in acute asthma; therefore, monitoring by serum IL-8 concentration is of limited value. The clinical value of serum IL-8 as a marker of disease activity remains to be established.
J Asthma 2000 Aug
PMID:Evaluation of serum interleukin-8 as a marker of disease activity in acute asthma in children. 1098 18

Cystic fibrosis (CF) is a complex multisystem disorder caused by mutations in a membrane glycoprotein called the CF transmembrane regulator (CFTR), which has as its major function serving as a Cl- channel. The relationship between defects in CFTR and development of lung disease remains incompletely understood. Chronic lung disease, characterized by persistent infection with a peculiar type of Pseudomonas aeruginosa, bronchiectasis, and airway obstruction is the major cause of morbidity and mortality in CF patients. The inflammatory response to the chronic infection resembles that induced by lipopolysaccharide (LPS) and is mediated primarily by cytokines such as tumor necrosis factor (TNF), interleukin-1 (IL-1), IL-6, and IL-8, whose synthesis is activated by the transcription factor nuclear factor kappa B (NF-kappa B). Large numbers of neutrophils dominate the inflammatory response and excessive concentrations of their products create a vicious cycle that becomes injurious rather than protective and eventually claims the life of the patient.
Allergy Asthma Proc
PMID:Inflammatory mediators in cystic fibrosis lung disease. 1189 30

In recent years, increasing evidence has indicated an important role for T cells in various drug-induced diseases. A detailed analysis of patients with various drug allergies revealed the existence of drug-specific T cells in the circulation or in eluate from skin infiltration in bullous, pustular, and maculopapular drug eruptions. The drug-specific T cells use the ab-T cell receptor CD4+ or CD8+ and react with drugs acting as haptens (covalently bound to larger molecules, such as penicillins), but also recognize drugs if they are bound only in a labile way to major histocompatibility complex molecules (noncovalent drug presentation). Functional analysis revealed a predominant IL-5 production by drug-specific CD4+ T cells in maculopapular exanthema (MPE) and bullous skin diseases, while patients with acute generalized exanthematous pustulosis have a peculiar T cell subset secreting high amounts of IL-8. Moreover, in MPE CD4+, perforin+ T cells were found in vitro and in immunohistology that had cytotoxic potential and killed keratinocytes in vitro and in vivo.
Curr Allergy Asthma Rep 2002 Jan
PMID:T cells in drug allergy. 1189 20

Interleukin (IL)-16 is a homotetramer of 14-kDa subunits discovered in 1982 as a T-cell-specific chemoattractant factor. IL-16 plays a role in trafficking of several immune cells and may be a major chemotactic signal for CD4+ cells. Here, we review some of the key biological actions of IL-16. Because this cytokine has been shown to affect the levels of many inflammatory mediators such as histamine, serotonin, regulated upon activation, normal T cell expressed and secreted (RANTES), and monocyte chemotactic protein-1 (MCP-1), and other cytokines such as IL-2, we investigated the effect of IL-16 on control and stimulated human umbilical cord blood-derived cultured mast cells after antigen challenge. We found that human recombinant IL-16 (0.2-200 ng/mL) does not affect either basal tryptase or IL-8 release or that induced by anti-immunoglobulin E activation. In accordance with other data in the medical literature, we conclude that the most important function of IL-16 is the chemoattraction of CD4+ cells.
Allergy Asthma Proc
PMID:Interleukin-16 network in inflammation and allergy. 1200 88

The aim of this study was to compare the degree of inflammation present in acute sinusitis, allergic rhinitis, chronic Fatigue Syndrome (CFS), and non-CFS control subjects by measuring cytokine concentrations in nasal lavage fluids. The concentrations of total protein (TP; Lowry assay), nerve growth factor (NGF), tumor necrosis factor (TNF) alpha, and interleukin (IL)-8 were measured by ELISA in nasal lavage fluids from acute sinusitis (n = 13), active allergic rhinitis (n = 16), CFS (n = 95), and non-CFS (n = 89) subjects. CFS and non-CFS groups were subdivided further using allergy skin test and rhinitis score results. Acute sinusitis subjects had significantly higher TP (p = 0.011, ANOVA), TNF-alpha (p = 0.00071), and IL-8 (p = 0.0000027) concentrations and IL-8/TP ratios (p = 0.0030) than the other three patient groups. There were no differences based on skin test or rhinitis score severity within either the CFS or non-CFS groups. The mucopurulent discharge of acute sinusitis contained significantly higher TNF-alpha and IL-8. Neutrophils were a likely source for these cytokines. There were no differences between CFS and non-CFS subjects, making it unlikely that the rhinitis of CFS has an inflammatory component.
Allergy Asthma Proc
PMID:Cytokines in nasal lavage fluids from acute sinusitis, allergic rhinitis, and chronic fatigue syndrome subjects. 1212 6

The aqueous extract of propolis has been formulated as a nutritional food product and administered, as an adjuvant to therapy, to patients with mild to moderate asthma daily for 2 months in the framework of a comparative clinical study in parallel with a placebo preparation. The diagnosis of asthma was made according to the criteria of patient classification of the National Institutes of Health and Global Initiative for Asthma Management. At inclusion, the pulmonary forced expiratory volume in the first second (FEV1) as a percentage of the forced vital capacity (FVC) was more than 80% in mild persistent cases, and between 60 and 80% in moderate persistent cases, showing an increase in the degree of reversibility of > 15% in FEV1. All patients were on oral theophylline as controller therapy, none was receiving oral or inhaled corticosteroids, none had other comorbidities necessitating medical treatment, and all were from a middle-class community and had suffered from asthma for the last 2-5 years. Twenty-four patients received the placebo, with one drop-out during the study, while 22 received the propolis extract, with no drop-outs. The age range of the patients was 19-52 years; 36 were male and 10 female. The number of nocturnal attacks was recorded on a weekly basis, while pulmonary function tests were performed on all patients at the beginning of the trial, 1 month later and at the termination of the trial. Immunological parameters, including various cytokines and eicosanoids known to play a role in asthma, were measured in all patients at the beginning of the trial and 2 months later. Analysis of the results at the end of the clinical study revealed that patients receiving propolis showed a marked reduction in the incidence and severity of nocturnal attacks and improvement of ventilatory functions. The number of nocturnal attacks dropped from an average of 2.5 attacks per week to only 1. The improvement in pulmonary functions was manifested as a nearly 19% increase in FVC, a 29.5% increase in FEV1, a 30% increase in peak expiratory flow rate (PEFR), and a 41% increase in the forced expiratory flow rate between 25 and 75% of the vital capacity (FEF25-75). The clinical improvement was associated with decreases by 52, 65, 44 and 30%, respectively, of initial values for the pro-inflammatory cytokines tumor necrosis factor (TNF)-alpha, ICAM-1, interleukin (IL)-6 and IL-8, and a 3-fold increase in the 'protective' cytokine IL-10. The levels of prostaglandins E2 and F2alpha and leukotriene D4 were decreased significantly to 36, 39, and 28%, respectively, of initial values. Patients on the placebo preparation showed no significant improvement in ventilatory functions or in the levels of mediators. The findings suggest that the aqueous propolis extract tested is potentially effective as an adjuvant to therapy in asthmatic patients. The benefits may be related to the presence in the extract of caffeic acid derivatives and other active constituents.
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PMID:A clinical pharmacological study of the potential beneficial effects of a propolis food product as an adjuvant in asthmatic patients. 1258 35

The aim of the study was to investigate the activation of inflammatory mediators interleukin (IL)-4, IL-5, and IL-8; immunoglobulin E (IgE); and eosinophil cationic protein (ECP) and to evaluate the regulatory role of the tumor necrosis system (TNF) system in bronchial hyperreactivity. Adults who had suffered from bronchial asthma in childhood but who had been symptom free for at least 3 years were examined together with their children who did not have asthma. The serum concentrations of TNF-alpha, soluble TNF receptor 1 (sTNF-R1), TNF-R2, IL-4, IL-5, IL-8, ECP, and IgE were studied in symptom-free adults (n = 22) and their children (n = 22) with bronchial hyperreactivity. Nonhyperreactive individuals with a similar medical history (adults, n = 17; children, n = 20) served as controls. Significantly elevated serum TNF-alpha (X +/- SD: 5.13 +/- 1.37 pg/mL versus 3.91 +/- 0.61 pg/mL; p < 0.0001), sTNF-R1 (X +/- SD: 1.37 +/- 0.28 ng/mL versus 1.16 +/- 0.13 ng/mL; p = 0.0002), and sTNF-R2 (X +/- SD: 0.78 +/- 0.42 ng/mL versus 0.43 +/- 0.41 ng/mL; p = 0.0001); IL-4 (X +/- SD: 4.05 +/- 1.02 pg/mL versus 3.34 +/- 0.84 pg/mL; p = 0.0016); IgE (X +/- SD: 390.1 +/- 361.4 KU/L versus 130.2 +/- 166.1 KU/L; p = 0.0001); and ECP (X +/- SD: 17.57 +/- 11.03 micrograms/L versus 10.65 +/- 6.01 micrograms/L; p = 0.0016) concentrations were measured in the subjects with bronchial hyperreactivity as compared with the nonhyperreactive group. Significant positive linear correlations were observed for the bronchial hyperreactive group between the concentrations of TNF-alpha and ECP, TNF-alpha and sTNF-R1, TNF-alpha and IL-8, sTNF-R1 and ECP, sTNF-R1 and IL-8, and sTNF-R2 and IL-8. Moreover, the TNF-alpha and sTNF-R2 levels correlated with the airway reactivity in the hyperreactive group. We suggest that the elevated cytokine levels indicate activation of the immune system in individuals who were previously asthmatic, but recovered, and are now symptom free and in their children with nonasthmatic bronchial hyperreactivity. The TNF system may play a key role in the pathomechanism of bronchial hyperreactivity.
Allergy Asthma Proc
PMID:Relationship between the tumor necrosis factor system and the serum interleukin-4, interleukin-5, interleukin-8, eosinophil cationic protein, and immunoglobulin E levels in the bronchial hyperreactivity of adults and their children. 1277 44

Conjunctival epithelial cells do not act only as mechanical barriers, preventing the entry of particles, bacteria, viruses, and noxious substances into the eye but they are also active participants in the regulation of allergic inflammation via expressing adhesion/effector molecules (intercellular adhesion molecule-1, vascular cell adhesion molecule-1, human leukocyte antigen-DR, CD40/CD40L, Fas/Fas ligand) on their surfaces and releasing numerous proinflammatory cytokines, such as eotaxin, regulated on activation normal T-cell expressed and released (RANTES), macrophage inflammatory protein-1, interleukin (IL)-8, IL-6, and tumor necrosis factor-a, which are necessary for the proliferation, differentiation, activation, and chemotaxis of various inflammatory cells into the conjunctiva. Histamine, released from the conjunctival mast cells, might stimulate the synthesis of proinflammatory molecules such as IL-6 and IL-8 by the epithelial cells through the receptors that couple to inositol phosphate generation and, therefore, amplify the allergic response. The relationship between the epithelium and allergy should be considered in detail in future studies aiming at an effective control and treatment of all forms of allergic conjunctivitis.
Curr Allergy Asthma Rep 2003 Jul
PMID:Epithelial cells in ocular allergy. 1279 Dec 15

Asthma is an inflammatory disease of the lungs and the transcription factor NF-kappa B regulates the production of numerous inflammatory mediators that may have a role in the pathogenesis of asthma. Hence, the signalling pathways leading to NF-kappa B activation are considered prime targets for novel anti-inflammatory therapies. The prevention of NF-kappa B activity in mice, through the knockout of IKK beta or p65, causes fatal liver degeneration in utero making it difficult to determine the full implications of inhibiting NF-kappaB activity in tissues physiologically relevant to human diseases. This study used adenovirus delivery of a dominant inhibitor of NF-kappaB (I kappa B alpha delta N) and dominant-negative IKK alpha (IKK alpha(KM)) and IKK beta (IKK beta(KA)) to investigate the role of the individual IKKs in NF-kappa B activation and inflammatory gene transcription by human pulmonary A549 cells. Overexpression of IKK beta(KA) or I kappa B alpha delta N prevented NF-kappa B-dependent transcription and DNA binding. IKK beta(KA) also prevented I kappa B alpha kinase activity. Similarly, IKK beta(KA) and I kappa B alpha delta N overexpression also inhibited IL-1beta- and TNF alpha-dependent increases in ICAM-1, IL-8 and GM-CSF in addition to IL-1beta-mediated increases in cyclooxygenase-2 expression, whereas IKK alpha(KM) overexpression had little effect on these outputs. IKK beta(KA) also reduced cell viability and induced caspase-3 and PARP cleavage regardless of the stimuli, indicating the induction of apoptosis. This effect seemed to be directly related to IKK beta kinase activity since I kappa B alpha delta N only induced PARP cleavage in TNF alpha-treated cells. These results demonstrate that inhibition of IKK beta and NF-kappa B suppresses inflammatory mediator production and reduces A549 cell viability. Thus, novel therapies that target IKK beta could have potent anti-inflammatory effects and may be beneficial in the treatment of certain cancers.
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PMID:Validation of IKK beta as therapeutic target in airway inflammatory disease by adenoviral-mediated delivery of dominant-negative IKK beta to pulmonary epithelial cells. 1572 90


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