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 infections in Japan have rapidly changed, because pathogenesis has also changed by the increase of compromised hosts and aged people with the development of chemotherapeutic agents and another medical progresses. Various respiratory infections have been accumulated in our clinical department and clinical investigations were done for these diseases during almost 20 years. Firstly, pneumonias in adult T cell leukemia have been very severe and these diseases have occurred with load from pathogenic orophayngeal bacteria to lower respiratory airway. With another clinical studies, these pathogenesis which firstly pathogenic bacteria attach to orophayngeal epithelial cells and would move to lower respiratory airway to infect were given very clear evidences especially for Branhamella and Pneumococcus infections with chronic respiratory infections. The exact clearance of pathogenic orophayngeal bacteria using povidon iode solution was very useful for prevention of these acute or chronic respiratory infections. Although acute bronchitis is very popular, the secondary bacterial pathogens remained to be unknown, in the world. We showed that H. influenzae, S.pneumoniae and B.catarrhalis were common major pathogens as the secondary invading bacteria of acute bronchitis in Japan, Thailand and Bangladesh. Recently, the pathogenesis of severe chronic respiratory infections such as diffuse panbronchiolitis is focused after the development of erythromycin therapy. We gave some evidences of macrolides effectiveness which these drugs inhibited IL-8 production. We described the importance of inflammatory cell classification in sputa or bronchial secretions for deep understanding of inflammatory situation in broncho-bronchiolar airway.(ABSTRACT TRUNCATED)
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PMID:[Respiratory infections--pathogenesis of acute and chronic infections]. 883 Nov 94

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

Hypersensitivity pneumonitis (HP) is a granulomatous, inflammatory lung disease caused by inhalation of organic Ags, most commonly thermophilic actinomycetes that cause farmer's lung disease. The early response to Ag is an increase in neutrophils in the lung, whereas the late response is a typical Th1-type granulomatous disease. Many patients who develop disease report a recent viral respiratory infection. These studies were undertaken to determine whether viruses can augment the inflammatory responses in HP. C57BL/6 mice were exposed to the thermophilic bacteria Saccharopolyspora rectivirgula (SR) for 3 consecutive days per wk for 3 wk. Some mice were exposed to SR at 2 wk after infection with respiratory syncytial virus (RSV), whereas others were exposed to SR after exposure to saline alone or to heat-inactivated RSV. SR-treated mice developed a typical, early neutrophil response and a late granulomatous inflammatory response. Up-regulation of IFN-gamma and IL-2 gene expression was also found during the late response. These responses were augmented by recent RSV infection but not by heat-inactivated RSV. Mice with a previous RSV infection also had a greater early neutrophil response to SR, with increased macrophage inflammatory protein-2 (MIP-2, murine equivalent of IL-8) release in bronchoalveolar lavage fluid. These studies suggest that viral infection can augment both the early and late inflammatory responses in HP.
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PMID:Viral infection modulates expression of hypersensitivity pneumonitis. 1035 92

Respiratory infection by Actinobacillus pleuropneumoniae causes a highly pathogenic necrotizing pleuropneumonia with severe edema, hemorrhage and fever. Acute infection is characterized by expression of inflammatory cytokines, including interleukin-1 (IL-1), IL-6 and IL-8. To determine if high level production of inflammatory cytokines contributed to disease pathogenesis, we investigated if inhibiting macrophage activation with adenovirus type 5-expressed IL-10 (Ad-5/IL-10) reduced the severity of acute disease. Porcine tracheal epithelial cells infected with Ad-5/IL-10 produced bioactive human IL-10. When pigs were intratracheally infected with A. pleuropneumoniae, pigs pretreated with Ad-5/IL-10 showed a significant reduction in the amount of lung damage when compared to adenovirus type 5-expressing beta-galactosidase (Ad-5/beta-Gal)-treated and untreated pigs. In addition, serum zinc levels were unchanged, the lung weight/body weight ratio (an indicator of vascular leakage) was significantly reduced, and lung pathology scores were reduced. Myeloperoxidase activity in lung lavage fluid samples, an indicator of neutrophil invasion, was decreased to levels similar to that seen in pigs not infected with A. pleuropneumoniae. Reduction in inflammatory cytokine levels in lung lavage fluid samples correlated with the clinical observations in that pigs pretreated with Ad-5/IL-10 showed a corresponding reduction of IL-1 and tumor necrosis factor (TNF) compared with untreated and Ad-5/beta-Gal-treated pigs. IL-6 levels were unaffected by pretreatment with Ad-5/IL-10, consistent with observations that IL-6 was not derived from alveolar macrophages. Since inflammatory cytokines are expressed at high levels in acute bacterial pleuropneumonia, these results indicate that macrophage activation, involving overproduction of IL-1 and TNF, is a prime factor in infection-related cases of massive lung injury.
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PMID:Interleukin-10 gene therapy-mediated amelioration of bacterial pneumonia. 1089 82

Neonatal exanthematous diseases induced by toxic shock syndrome toxin-1 (TSST-1)-producing methicillin-resistant Staphyloccocus aureus (MRSA) is one of emerging infectious diseases in Japan. We experienced 36 patients with this disease in National Kagawa Children's Hospital and in 13 patients of them, investigated the role of both the toxin and cytokines in pathogenesis of it. The results are summarized as follows: 1. The TSST-1 level was high in the umbilical inflammatory exudate of cases induced by umbilical infection and in the gastric fluid of cases induced by respiratory infection. The blood TSST-1 level was below the detection limit in most of the exathematous++ cases examined, but it was detected in one of the nine cases induced by respiratory infection and a case secondary to severe MRSA infection (phlegmonous abscess in buttock). 2. Local cytokine levels were examined in the abscess pus obtained from a case of severe MRSA infection and in the gastric fluid from cases induced by respiratory infection. The local levels of TNF [alpha], IL-1 [beta], IL-6 and IL-8 were markedly high, but the local levels of IL-2 and IFN-[gamma] were similar to their blood levels. 3. The severity of hypercytokinemia (IL-1 [beta], IL-2, IL-6, IFN-[gamma]) was proportionate to the severity of exanthematous disease. Accompanied by increased levels of inhibitory factors sTNF-R, IL-1 ra, sIL-2R and IL-10, this hypercytokinemia normalized soon within four or five days. 4. As compared to cases induced by umbilical infection, cases induced by respiratory infection often had higher blood cytokine levels and some of them had cardiorespiratory disorders. Based on the results of this study, we consider that this disease is generally induced by toxemia with a small number of toxins without tissue destructive lesions by MRSA infection and that this is closely related to the course of the disease that shows a tendency to a spontaneous recovery.
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PMID:[A new exanthematous disease in newborn infants caused by exotoxins producing methicillin-resistant Staphylococcus aureus; pathology from viewpoints of local and systemic levels of exotoxin and cytokine]. 1096 60

Interleukin-8 (IL-8) is considered as the major polymorphonuclear neutrophils (PMNs) chemoattractant cytokine in lung diseases such as asthma and adult respiratory distress syndrome (ARDS). However, controversial results were obtained regarding the involvement of IL-8 in the pathogenesis of pneumonia. This study examines the role of IL-8 in the recruitment and activation of PMNs in the lung of pneumonia patients. The interesting aspect of this study is that it is a site- specific analysis of the infected and uninfected lungs of the same patient. The level of IL-8 mRNA, protein and myeloperoxidase present in the cells of the bronchioalveolar lavages (BALs) taken from the areas of known pneumonic consolidations on chest X-ray (infected lung) are compared with the BALs obtained from areas of no obvious infiltrate (non-infected lung). The results obtained from the infected and non-infected lungs of pneumonic patients were further compared with that of a control group of non-smoking patients. The level of IL-8 mRNA and protein were determined by RT-PCR and ELISA respectively. There was a significant increase in the level of IL-8 mRNA in the infected lung as compared to its level in the non-infected lung (p < 0.001). In correlation with the increase in mRNA, IL-8 protein concentrations in BAL fluids from the infected lung were 6 fold higher than those taken from the non-infected lung (p < 0.0001). This pattern was also consistent with MPO activity in the BALs (4.5 fold more MPO activity in the infected lung as compared to that of the non-infected lung), indicating that IL-8 is directly implicated in neutrophil accumulation that follows acute respiratory infection. The results of the present study, therefore, indicate the involvement of IL-8 in the pathogenesis of pneumonia.
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PMID:Levels of IL-8 and myeloperoxidase in the lungs of pneumonia patients. 1126 53

Because Mycoplasma pneumoniae is hypothesized to play an important role in reactive airway disease/asthma, a comprehensive murine model of M. pneumoniae lower respiratory infection was established. BALB/c mice were intranasally inoculated once with M. pneumoniae and sacrificed at 0 to 42 days postinoculation. All mice became infected and developed histologic evidence of acute pulmonary inflammation, which cleared by 28 days postinoculation. By contrast, M. pneumoniae persisted in the respiratory tract for the entire 42 days studied. Tumor necrosis factor alpha, gamma interferon, interleukin-6 (IL-6), KC (functional IL-8), MIP-1alpha, and MCP-1/JE concentrations were significantly elevated in bronchoalveolar lavage samples, whereas IL-4 and IL-10 concentrations were not significantly elevated. Pulmonary airflow resistance, as measured by plethysmography, was detected 1 day postinoculation and persisted even after pulmonary inflammation had resolved at day 28. Serum anti-M. pneumoniae immunoglobulin G titers were positive in all mice by 35 days. This mouse model provides a means to investigate the immunopathogenesis of M. pneumoniae infection and its possible role in reactive airway disease/asthma.
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PMID:Elevated cytokine and chemokine levels and prolonged pulmonary airflow resistance in a murine Mycoplasma pneumoniae pneumonia model: a microbiologic, histologic, immunologic, and respiratory plethysmographic profile. 1134 53

Respiratory infection is extremely common and a major cause of morbidity and mortality worldwide. The airway epithelium has an important role in host defense against infection and this is illustrated in this review by considering infection by respiratory viruses. In patients with asthma or chronic obstructive pulmonary disease, respiratory viruses are a common trigger of exacerbations. Rhinoviruses (RV) are the most common virus type detected. Knowledge of the immunopathogenesis of such RV-induced exacerbations remains limited, but information is available from in vitro and from in vivo studies, especially of experimental infection in human volunteers. RV infects and replicates within epithelial cells (EC) of the lower respiratory tract. EC are an important component of the innate-immune response to RV infection. The interaction between virus and the intracellular signaling pathways of the host cell results in activation of potentially antiviral mechanisms, including type 1 interferons and nitric oxide, and in the production of cytokines and chemokines [interleukin (IL)-1 beta, IL-6, IL-8, IL-11, IL-16, tumor necrosis factor alpha, granulocyte macrophage-colony stimulating factor, growth-regulated oncogene-alpha, epithelial neutrophil-activating protein-78, regulated on activation, normal T expressed and secreted, eotaxin 1/2, macrophage-inflammatory protein-1 alpha], which influence the subsequent induced innate- and specific-immune response. Although this is beneficial in facilitating clearance of virus from the respiratory tract, the generation of proinflammatory mediators and the recruitment of inflammatory cells result in a degree of immunopathology and may amplify pre-existing airway inflammation. Further research will be necessary to determine whether modification of EC responses to respiratory virus infection will be of therapeutic benefit.
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PMID:Host defense function of the airway epithelium in health and disease: clinical background. 1297 16

The obligate intracellular bacterial pathogen Chlamydia pneumoniae (Cp) is responsible for a range of human diseases, including acute respiratory infection. Although experimental intratracheal infection with Cp results in a massive recruitment of neutrophil granulocytes (polymorphonuclear neutrophils (PMN)), the role of these cells in the defense against Cp is unclear. In this study the interactions of PMN with Cp were investigated. In vitro coincubation experiments showed that human granulocytes were able to internalize Chlamydia in an opsonin-independent manner. Importantly, phagocytosed Cp were not killed; the ingested bacteria survived and multiplied within PMN. Although uninfected granulocytes became apoptotic within 10 h, infected PMN survived up to 90 h. Coincubation with Cp significantly decreased the ratio of apoptotic PMN, as detected by morphological analysis, annexin V, and TUNEL staining. The observed antiapoptotic effect was associated with a markedly lower level of procaspase-3 processing and, consequently, reduced caspase-3 activity in infected PMN. LPS was found as a major, but not exclusive, component responsible for the observed antiapoptotic effect. Chlamydia LPS affected PMN apoptosis both by acting directly on the cells and by inducing the autocrine production of the antiapoptotic cytokine IL-8. These data show that, in contrast to other microbial pathogens that drive phagocytes into apoptosis to escape killing, Cp can extend the life span of neutrophil granulocytes, making them suitable host cells for survival and multiplication within the first hours/days after infection.
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PMID:Chlamydia pneumoniae multiply in neutrophil granulocytes and delay their spontaneous apoptosis. 1473 60

Respiratory infections are very frequent in children. Bacillus clausii has been demonstrated to exert some immunomodulatory activities and to be safe. We conducted a study to investigate whether B. clausii administration in allergic children with recurrent respiratory infections might modulate cytokine pattern. Ten children (mean age 4.4 yr) attending the nursery school were enrolled at the end of school year (i.e. in the summer). Bacillus clausii spores (Enterogermina): 2 billion spores per vial) were administered at the dosage schedule of two vials a day for 4 wk. A panel of cytokines, including interleukin (IL)-1, IL-3, IL-4, IL-6, IL-8, IL-10, IL-12, interferon (IFN)-gamma, transforming growth factor (TGF)-beta, and tumor necrosis factor (TNF)-alpha, was measured by immunoassay in the fluid recovered from nasal lavage, performed before and after the treatment. Bacillus clausii treatment induced a significant decrease of IL-4 levels (p < 0.01) and a significant increase of IFN-gamma (p < 0.05), IL-12 (p < 0.001), TGF-beta (p < 0.05), and IL-10 (p < 0.05) levels. Other cytokines were not significantly modified. In conclusion, this study shows that the B. clausii may exert immunomodulating activity by affecting cytokine pattern at nasal level in allergic children with recurrent respiratory infections.
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PMID:Cytokines evaluation in nasal lavage of allergic children after Bacillus clausii administration: a pilot study. 1505 91


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