Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the last decade, the method of sputum induction (SI) has offered the opportunity to study inflammation in patients with chronic obstructive pulmonary disease (COPD). This paper reviews methodological aspects of SI and summarizes its uses in the research of inflammation in COPD, including sputum cellularity and soluble markers. SI is a relatively safe, reliable, and reproducible technique, used to investigate different aspects of airway inflammation. Although various methods of induction and processing have been proved safe and highly reproducible, a generally accepted method is needed. Sputum analysis has given evidence for increased numbers of macrophages and neutrophils in COPD patients compared to normal subjects. In some studies, increased numbers of eosinophils have been also reported. Changes in various mediators have been found in sputum supernatant of COPD patients (IL-8, LTB-4 and TNF-a). The clinical usefulness of the method in the follow-up of the disease has not been explored extensively. A number of observations in patients with different clinical characteristics could be proven useful in identifying patterns of inflammation associated with different prognosis. Finally, SI could also guide treatment; such as, sputum eosinophilia in COPD could predict response to inhaled corticosteroids.
 ...
PMID:Induced sputum in the investigation of airway inflammation of COPD. 1292 12

The aim of this study was to investigate potential differences in the local nasal immune response between bronchiolitis and upper respiratory tract infection induced by respiratory syncytial virus (RSV). Nasal brush samples were obtained from 14 infants with RSV bronchiolitis and from 8 infants with RSV upper respiratory tract infection. The samples were taken during infection (acute phase) and 2-4 weeks later (convalescent phase). Cytospin preparations were stained immunohistochemically for T cells, macrophages, and eosinophils. Staining also took place for intercellular adhesion molecule-1 (ICAM-1), T-helper 1 (Th1)-like (interleukin-12 [IL-12], interferon-gamma [IFN-gamma]), Th2-like (IL-4, IL-10), and proinflammatory cytokines (IL-6, IL-8, IL-18). During both RSV-induced bronchiolitis and upper respiratory tract infection, cellular inflammation was observed. This was characterised by an increase in the numbers of nasal macrophages, which tended to be higher in bronchiolitis than in upper respiratory tract infection. Numbers of T lymphocytes and ICAM-1 positive cells increased during both bronchiolitis and upper respiratory tract infection. There were no differences between numbers in the groups. Interestingly, a distinct nasal proinflammatory cytokine response was observed in RSV-induced bronchiolitis. This is characterised by an increase in the number of IL-18 positive cells. This increase is specific for bronchiolitis, as a similar increase could not be detected in RSV-induced upper respiratory tract infection. Numbers of IL-6 and IL-12 positive cells were higher in both bronchiolitis and upper respiratory tract infection, and there were no differences between the groups. By contrast, the number of IL-8, IFN-gamma, IL-4, and IL-10-positive cells remained constant. In conclusion, clear differences were found in nasal immune responses of children with RSV-induced upper respiratory tract infection or bronchiolitis. The induction of a strong IL-18 response was typical for bronchiolitis, as this could not be observed in RSV-induced upper respiratory tract infection, and could explain the eosinophilia that is observed frequently during bronchiolitis.
 ...
PMID:RSV-induced bronchiolitis but not upper respiratory tract infection is accompanied by an increased nasal IL-18 response. 1293 5

OBJECTIVE: The aims of this study were to evaluate inflammatory cells, the profile of inflammatory mediators in nasal lavage (NL), and the involvement of the paranasal mucosa in atopic infants with no symptoms of sinusitis. METHODS: 48 atopic patients with allergic rhinitis (AR), and 33/48 patients with asthma were studied; the control group consisted of 13 nonatopic children. Those individuals with acute, chronic or recurrent sinusitis were excluded. The involvement of the paranasal mucosa was assessed by coronal computed tomography (CT) and graded by a standard protocol (0-30). A CT score greater than or equal to 12 indicated extensive involvement. Nasal lavage was used to quantify total and differential nasal cell counts. An aliquot of the supernatant was used for determining inflammatory mediators: interleukin-8 (IL-8), myeloperoxidase (MPO), and eosinophil cationic protein (ECP). Albumin was used as a marker for increased vascular permeability. These measurements were performed on all of the atopic patients and in 6/13 patients in the control group. The three groups were submitted to spirometry and complete blood cell count. RESULTS: Extensive involvement of the paranasal mucosa was observed in 7/33 (21%) of asthmatic patients (Group I) and 2/15 (13%) of those with allergic rhinitis (Group II). The highest CT score in the control group (Group III) was 7. Total cell and eosinophil count/ml and albumin concentration in nasal fluid were higher in asthmatic patients whose CT score was greater than 12. Interleukin-8 concentration, number of neutrophils and epithelial cells/ml in nasal fluid were similar in the three groups. A positive correlation between CT score, peripheral blood eosinophilia, number of eosinophils/ml and eosinophil cationic protein concentration was found in the nasal fluid of atopic children (n=48). There was an association between number of neutrophils and titers of interleukin-8 and myeloperoxidase, and between interleukin-8 and eosinophil count. CONCLUSIONS: in asthmatic patients with no symptoms of sinusitis, the extensive involvement of the paranasal mucosa is associated with blood and nasal lavage eosinophilia and cellular activation. Neutrophil infiltration and activation were not related to increased involvement of the paranasal mucosa.
 ...
PMID:[Inflammatory mediators, cell counts in nasal lavage and computed tomography of the paranasal sinuses in atopic children] 1464 58

Nasal polyps are characterized by eosinophilic infiltration and presence of inflammatory mediators, such as total IgE, eosinophil cationic protein (ECP) and cytokines. The role of atopy in nasal polyp pathogenesis is still unclear. Therefore, we evaluated serum IgE levels, nasal mucus concentrations of ECP and cytokines and the number of infiltrating eosinophils in nasal tissue of polyps from atopic and non-atopic patients. Samples were obtained from a randomized population of 31 patients with nasal polyposis having endonasal sinus surgery and of 13 control subjects undergone corrective surgery of the nasal septum. On the basis of medical history of allergy, positive skin-prick tests and total IgE levels, patients with polyposis were divided in atopic (n = 13) and non-atopic (n = 18) patients. We determined levels of IgE in blood, ECP and cytokines (IL-4, IL-6, IL-8, IFN-gamma and IL-2) in nasal mucus, and number of infiltrating eosinophils in nasal tissue. The concentrations of total IgE, ECP, IL-4 and IL-8 and eosinophilia were significantly higher in all patients with nasal polyps compared with controls. Inside, all patients with nasal polyposis showed lower levels of IL-6, IFN-gamma and IL-2 compared with controls. The atopic patients showed significant differences when compared with non-atopic patients for the higher concentrations of total IgE (698.80+/-322.24 vs. 279.63+/-234.11; P < 0.0001) and IL-8 (1437.2 pg/ml+/-1250.7 vs. 605.5 pg/ml+/-481.1; P < 0.015). These findings suggest that inflammation still remains the major factor in the etiology of nasal polyposis and show different levels of inflammatory mediators into atopic and non-atopic patients.
 ...
PMID:Inflammatory mediators and eosinophilia in atopic and non-atopic patients with nasal polyposis. 1593 9

Allergic bronchopulmonary aspergillosis (ABPA) is a complication of persistent asthma and cystic fibrosis (CF), diseases in part characterized by excessive viscous mucus and compromised mucociliary clearance. Inhaled conidia of Aspergillus fumigatus are able to persist and germinate, releasing exoproteases and other fungal products that further compromise clearance, breach the epithelium, and activate immune responses. Chemotactic cytokines (e.g. IL-8, RANTES, eotaxin) in particular have been implicated in murine models. Chemokine-mediated recruitment of CD4+TH2 lymphocytes specific for A. fumigatus is a crucial feature of ABPA. Susceptibility also appears to involve immunogenetic factors including atopy and defined major histocompatibility complex-restricted allelic expression on antigen-presenting cells that are permissive for a TH2-predominant immune response. Certain A. fumigatus allergens appear more associated with ABPA rather than simple A. fumigatus allergy. ABPA is characterized by marked local and systemic eosinophilia, an adaptive immune response with elevated levels of A. fumigatus-specific IgG, IgA and IgE antibodies, and a profound nonspecific IL-4-dependent elevation in total IgE. Clinically, ABPA manifests with recurring episodes of asthma, pulmonary infiltrates, and central bronchiectasis that may progress to fibrosis. It is treated with systemic glucocorticoids and azoles. Monitoring clinical, radiographic and serologic responses (especially total IgE) is essential for successful management.
 ...
PMID:Pathophysiology and immunology of allergic bronchopulmonary aspergillosis. 1611 Aug 13

Chronic obstructive pulmonary disease (COPD) is characterised by chronic obstruction of expiratory flow affecting peripheral airways, associated with chronic bronchitis (mucus hypersecretion with goblet cell and submucosal gland hyperplasia) and emphysema (destruction of airway parenchyma), together with fibrosis and tissue damage, and inflammation of the small airways. Inflammatory mediators include lipid mediators, chemokines, cytokines, growth factors, reactive oxygen species and proteinases. Increased levels of interleukin (IL)-6, IL-1beta, tumour necrosis factor-alpha (TNF-alpha) and IL-8 have been measured in sputum, with further increases during exacerbations, and the bronchiolar epithelium over-expresses MCP-1 and IL-8. IL-8 and LTB4 can account for neutrophil chemotactic activity of sputum. The expression of chemokines such as RANTES and eotaxin may underlie the airway eosinophilia observed in some COPD patients. Reactive oxygen species can increase gene expression of many inflammatory mediators, such as IL-1 and TNFalpha from macrophages, alveolar and bronchial epithelial cells. TNFalpha and IL-1beta stimulate macrophages to produced matrix metalloproteinase-9 (MMP-9), and bronchial epithelial cells to produce extracellular matrix glycoproteins such as tenascin. Increased expression of transforming growth factor-beta (TGFbeta) and of epidermal growth factor (EGF) occurs in the epithelium and submucosal cells of patients with chronic bronchitis. TGFbeta and EGF activate proliferation of fibroblasts, while activation of the EGF receptor leads to mucin gene expression.
 ...
PMID:Inflammatory mediators in chronic obstructive pulmonary disease. 1730 18

Reversal of eosinophilic inflammation has been an elusive therapeutic goal in the management of asthma pathogenesis. In this regard, GM-CSF is a primary candidate cytokine regulating eosinophil activation and survival in the lung; however, its molecular mechanism of propagation and maintenance of stimulated eosinophil activation is not well understood. In this study, we elucidate those late interactions occurring between the GM-CSF receptor and activated eosinophil signaling molecules. Using coimmunoprecipitation with GM-CSF-stimulated eosinophils, we have identified that the GM-CSF receptor beta-chain (GMRbeta) interacted with ICAM-1 and Shp2 phosphatase, as well as Slp76 and ADAP adaptor proteins. Separate experiments using affinity binding with a tyrosine-phosphorylated peptide containing an ITIM (ICAM-1 residues 480-488) showed binding to Shp2 phosphatase and GMRbeta. However, the interaction of GMRbeta with the phosphorylated ICAM-1-derived peptide was observed only with stimulated eosinophil lysates, suggesting that the interaction of GMRbeta with ICAM-1 required phosphorylated Shp2 and/or phosphorylated GMRbeta. Importantly, we found that inhibition of ICAM-1 in activated eosinophils blocked GM-CSF-induced expression of c-fos, c-myc, IL-8, and TNF-alpha. Moreover, inhibition of ICAM-1 expression with either antisense oligonucleotide or an ICAM-1-blocking Ab effectively inhibited ERK activation and eosinophil survival. We concluded that the interaction between ICAM-1 and the GM-CSF receptor was essential for GM-CSF-induced eosinophil activation and survival. Taken together, these results provide novel mechanistic insights defining the interaction between ICAM-1 and the GM-CSF receptor and highlight the importance of targeting ICAM-1 and GM-CSF/IL-5/IL-3 receptor systems as a therapeutic strategy to counter eosinophilia in asthma.
 ...
PMID:Cross-talk between ICAM-1 and granulocyte-macrophage colony-stimulating factor receptor signaling modulates eosinophil survival and activation. 1832 30

Diesel exhaust particles (DEPs), comprised mainly of particles less than 2.5 microm (PM 2.5) in aerodynamic diameter, have been assumed to enhance the response of asthma to allergen inhalation. Although eosinophilic infiltration is remarkable in the event of bronchial asthma induced by DEPs, the precise mechanisms leading to eosinophilia are unknown. To examine the effect of DEPs on eosinophils, we measured the cytokine products and activity of nuclear factor-kappa B (NF-kappa B) after addition of the proteasomal inhibitor MG132 in HL-60 clone 15 cells differentiated into eosinophils. We measured eotaxin-induced chemotaxis of cells and their activity of p38 mitogen-activated protein (MAP) kinase was analysed. Interleukin (IL)-8 and monocyte chemoattractant protein-1 (MCP-1) were increased markedly in DEPs-treated cells. The active form of NF-kappaB in cells treated with DEPs was increased, and this effect was significantly decreased by the administration of MG132. Cell migration in the presence of DEPs was significantly greater, and inhibited by adding N-acetyl l-cysteine. P38 MAP kinase activity was highly influenced by DEPs-treatment. DEPs induce MCP-1 and IL-8 production by up-regulating NF-kappa B activity, which is inhibited in the presence of an inhibitor of proteasomal degradation. DEP also promotes eotaxin-induced chemotaxis in a p38-dependent manner.
 ...
PMID:In vitro toxicity evaluation of diesel exhaust particles on human eosinophilic cell. 1835 85

Type IV of hypersensitivity reaction is usually manifested in the skin in different clinical pattern. According to traditional Gell and Coombs classification, the mechanism of IV type of allergic reaction has been associated with contact allergy with the activity of lymphocytes Th1 secreting interferon gamma. Now, this vision seems to be too simplified. In the last years there were publications, which can throw a new light on these complicated mechanisms leading to the development of the type IV of allergy, especially to drugs, nickel and other haptens and also can explain the differentiation of clinical pattern in respective patients. The skin symptoms in type IV of hypersensitivity are triggered by activation of specific T-cell CD4+ and CD8+. Immunohistochemical and functional analysis of reactive T-cell has shown that the delayed hypersensitivity reaction depends on the secreted cytokines. For example maculo-papular exanthema may be either triggered by Th1 or Th2 in nature and cytokines interferon gamma, tumor necrosis factor alfa or interleukin-4, 5 and 13. Bullous reactions (i.e. Stevens-Johnsons Syndrome or toxic epidermal necrolysis) are characterized by widespread keratinocyte apoptosis, a consequence of high CD8+ T-cell involvement and the molecular cytotoxicity of Fas, perforin and granzyme B. Pustular exanthema reactions are stimulated via the T-cell release of 11-8 and granulocyte-monocyte colony-stimulatig factor (GM-CSF). For the better understanding of these inflammatory cascades deleted type IV of hypersensitivity reactions have been re-classified into four main subtypes: 1. IVa with Th1 and monocyte directed and cytokines: IFNgamma, IL-1, IL-2, 2. IVb with Th2 and eosinophils directed and cytokines: L-5, IL-4, IL-13, 3. IVc with T CD8+ directed and cytokines: perforin, granzyme B, Fas Ligand, 4. IVd with T CD4+, CD8+ and neutrophil directed and cytokines: IL8, GM-CSF. Clinically delayed hypersensitivity eruptions are often an overlap of cytokine pathways, with one preferential reaction dominating the final picture. Type IVa and IVc play a role inthe mechanism of contact dermatitis, however type IV b in chronic asthma, chronic allergic rhinitis and maculo-papular exanthema with eosinophilia, type IV c in bullous reactions (i.e. Stevens-Johnsons Syndrome or toxic epidermal necrolysis), so type IV d in pustular exanthema reactions (i.g. AGEP - Acute Generalized Exanthematosus Pustule, Behcet disease). This different clinical pattern of allergic disease mainly including drug allergy to nickel and other haptens as well as chronic asthma and allergic rhinitis may be explained by above mechanisms. The study of different mechanisms of four subtypes of type IVof allergic reaction may be helpful in the differential diagnostics and in the treatment of allergic diseases.
 ...
PMID:[Type IV of hypersensitivity and its subtypes]. 1840 54

The present study aims to explore whether Mg infusion has a preventive effect on ischemia-reperfusion injury in rats. A total of 20 Sprague-Dawley-type adult male rats were used. In group 1 (control), 0.9% isotonic solution was administered. In group 2 (experiment), magnesium sulfate (0.5 mg per 100 g) was administered. Ischemia was induced for 15 min for the two groups. Magnesium (Mg), interleukin 8 (IL-8), and malondialdehyde levels were analyzed in blood, while edema, neutrophil infiltration, eosinophilia, loss of striation, and nucleolization were evaluated in histopathological examination. Mg levels in the experiment group were higher than those in the control group after ischemia-reperfusion (p < 0.05). In the control group, postischemia and postreperfusion IL-8 values were higher than preoperative values (p < 0.05). As for eosinophilia and loss of striation values, these were higher in the experiment group after ischemia-reperfusion than the values in the control group (p < 0.05). Histopathologically, Mg infusion cannot prevent the tissue injury triggered in ischemia-reperfusion periods. Eosinophilia can be one of the major and earliest markers of ischemia-reperfusion injury.
 ...
PMID:Preventive role of magnesium on skeletal muscle ischemia-reperfusion injury-an experimental study. 1880 32


<< Previous 1 2 3 4 5 6 Next >>