Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149514 (bronchitis)
 6,902 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chemical exposure may result in respiratory conditions such as chronic bronchitis, bronchial hyperresponsiveness, and chronic airway obstruction. Clinical studies have shown that during the course of disease, cytokine networks are changed. In order to study the relationship between blood cytokines and respiratory symptoms in an occupational setting, we investigated 106 chemical workers during a routine yearly medical examination in 1995. Lung function was measured with flow volume curves and impedance using the forced oscillation technique (FOT). Smoking-status and respiratory symptoms were determined by questionnaires. Cytokines were selected on biological plausibility and measured both in a whole blood assay (TNF-alpha, IL-8) and in serum (IL-4, IL-5, IL-6, IFN-gamma). The hypothesis is that blood levels of TNF-alpha and IL-8 are increased in bronchitis, while serum levels of IL4, IL-5 are increased and IFN-gamma is decreased in asthmatic workers. Spontaneous IL-8 release was significantly higher in workers with bronchitis (P < 0.05) or chronic bronchitis (P < 0.01) compared to workers without those respiratory symptoms, also after correction for age, pack-years, and blood lymphocyte numbers or compared to a matched control group. No correlation was present between specific cytokines and asthmatic symptoms. These data suggest that blood IL-8 may be considered as a useful marker for bronchitis.
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PMID:Blood interleukin-8 production is increased in chemical workers with bronchitic symptoms. 935 25

Some pulmonary diseases like bronchitis or asthma bronchiale are mediated by inflammatory mechanisms in bronchial epithelial cells. Alveolar macrophages are located directly in the surrounding of these cells, so that we suppose an interaction between epithelial cells and macrophages regarding to the release of inflammatory mediators. For measuring the contribution of macrophages to the release of inflammatory mediators by bronchial epithelial cells, we established an in vitro model of co-cultured blood monocytes (BM) and BEAS-2B cells in a transwell system (Costar). BM were exposed to Chrysotile B and soot particle FR 101 in a concentration of 100 microg/10(6) cells. After up to 90 min exposure time ELISA, EMSA (electromobility shift assay) and RT-PCR were used to measure protein tyrosine kinase activity, protein activity of NF-kappaB and cytokine (IL-1beta, IL-6, TNF-alpha) specific mRNA levels in BEAS-2B cells. We observed an increase in protein tyrosine kinase activity (up to 1.8 +/- 0.5-fold) and NF-kappaB protein activity in BEAS-2B cells after particle or fibre exposure of co-cultured BM. Consecutive IL-1beta-, IL-6- and TNF-alpha-mRNA were elevated (up to 1.9 +/- 0.58-fold). Protein tyrosine kinase activity, NF-kappaB activity, and the synthesis of cytokine-specific mRNA were inhibited by antioxidants. These data suggest a ROI-dependent NF-kappaB mediated transcription of inflammatory cytokines in bronchial epithelial cells.
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PMID:Reactive oxygen intermediate-release of fibre-exposed monocytes increases inflammatory cytokine-mRNA level, protein tyrosine kinase and NF-kappaB activity in co-cultured bronchial epithelial cells (BEAS-2B). 1042 62

Allergic diseases, atopy, bronchial asthma and chronic obstructive bronchitis are diseases which can directly or indirectly be traced to changes in the function of the immune system. Epidemiological studies have shown that these allergic diseases have increased in the course of time and that the incidence of obstruction of the respiratory system is clearly higher in polluted regions than in comparable control areas. These diseases are mainly the result of a comprehensive influence on the immune system. The present study describes the influence of pollutants on the behavior of cytokines which cannot be directly traced to an allergen or antigen in order to be able to explain various immunological or pseudo-allergic processes. We have isolated and cultivated PBMC from six donors and exposed them to different concentrations (5, 25, 50 and 100 mumol) of cadmium chloride. After incubation of cells with cadmium, different genes of cytokines were detected on the basis of mRNA by RT-PCR. Hsp70 can be detected in a relatively brief period following stress and there is an excellent correlation between heavy metal dose (stress) and expression of hsp70. In the case of IL-1, and TNF-alpha low concentrations of cadmium chloride increase the expression of these genes, whereas this effect is less noticeable with higher amounts of cadmium. After only one hour of exposure to heavy metals, large volumes of mRNA of IL-6 have been detected. IFN-gamma only reacts at high concentrations of cadmium. Heavy metals may influence immunocompetent cells so that they release several cytokines which may act on a large variety of cells in terms of a proinflammatory reaction. The influence of cytokines as well as the pollutants themselves on fibroblasts, endothelial cells as well as macrophages explains a number of processes which cannot be explained by allergical reactions. At low concentrations, cadmium is able to stimulate the immune system, while at higher concentrations inhibitory and suppressive reactions were observed.
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PMID:Influence of cadmium on the immune system. Description of stimulating reactions. 1076 26

The aim of this study was to investigate the cellular and biochemical events associated with repeated exposures to ozone. Twenty-three healthy subjects underwent single exposures to 200 ppb ozone and to filtered air (FA), as well as repeated exposures to 200 ppb ozone on 4 consecutive days, each for 4 h of intermittent exercise. Bronchoalveolar lavage was performed and mucosal biopsies were taken 20 h after the single or the last of the repeated exposures. As compared with FA, the single exposure to ozone caused a decrease in FEV(1), an increase in the percentages of neutrophils and lymphocytes, the concentrations of total protein, IL-6, IL-8, reduced glutathione, urate, and ortho-tyrosine in BAL fluid (BALF), but no changes in the cellular composition of biopsy. After the repeated exposure, the effect on lung function was abolished and differential cell counts in BALF were not significantly different from those after FA. However, the concentrations of total protein, IL-6, IL-8, reduced glutathione, and ortho-tyrosine were still increased. IL-10 could only be detected in BALF after repeated ozone exposures. Furthermore, macroscopic scores for bronchitis, erythema, and hypervulnerability of airway mucosa were increased, as well as numbers of neutrophils in bronchial mucosal biopsies. Our data demonstrate that airway inflammation persists after repeated ozone exposure, despite attenuation of some inflammatory markers in BALF and adaptation of lung function.
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PMID:The effect of repeated ozone exposures on inflammatory markers in bronchoalveolar lavage fluid and mucosal biopsies. 1085 57

Chlamydia pneumoniae is an obligate intracellular human pathogen that causes acute respiratory diseases such as pneumonia and bronchitis. Previous studies have established that C. pneumoniae can induce cytokines in mouse and/or human cells, but little information is available on the cytokine response of respiratory epithelial cells, a first line of infection. In this study, heparin treatment of C. pneumoniae significantly reduced its ability to induce interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-alpha) mRNA in human lung carcinoma cells, indicating that cytadherence is an important early stimulus for induction of proinflammatory mediators. Although the IL-8, gamma interferon, and TNF-alpha message was consistently induced by infection of A549 cells not treated with heparin, only an elevation of IL-8 protein was detected in A549 supernatants. A549 IL-beta and IL-6 mRNA and supernatant protein profiles were not significantly changed by infection. Heat or UV inactivation of C. pneumoniae only partially reduced the cytokine response, and inhibition of C. pneumoniae protein or DNA synthesis did not affect its ability to induce cytokine gene expression. To prevent stress-induced cytokine release by the A549 cells, centrifugation was not utilized for infection experiments. These experiments establish the importance of cytadherence in cytokine release by cells of respiratory epithelial origin and suggest that further work in the area of cytokine mediators is warranted to gain valuable pathogenic and therapeutic insights.
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PMID:Induction of proinflammatory cytokines in human lung epithelial cells during Chlamydia pneumoniae infection. 1254 May 37

Abnormal increments of pro-inflammatory cytokines (IL-6 and TNF-alpha) characterize the outbreak of infectious diseases, which are the major cause of death in the elderly. A counterbalance to the inflammation is exerted by IL-10 with an inhibitory role on TNF-alpha production. As is well known, some cytokine gene polymorphisms influence the cytokine production, playing a role as susceptibility or resistance factors against immune-mediated and infectious disease. Genetic variations in the -308A/G locus for TNF-alpha seems to affect the clinical outcome of some infectious diseases. In fact, the -308A allele is associated with severe septic shock and death. On this basis, we have screened healthy old subjects, nonagenarians and old patients affected by the acute phase of chronic obstructive bronchitis and bronchopneumonia of bacteria origin for the -308G/A locus (PCR-RFLP). Subjects are grouped in A+ (AG, AA genotypes) and A- (GG genotype) and data on IL-6, TNF-alpha, IL-10, NK cell cytotoxicity, zinc and metallothioneins (MTs) gene expression (RT-PCR) were stratified according to different TNF-alpha genotypes. The frequency of the A allele was increased in infected patients in comparison with healthy old controls. No differences existed between A+ and A- young adult, old and nonagenarian controls in tested parameters. Conversely, A+-infected patients displayed elevated IL-6, TNF-alpha and MTmRNA, low IL-10 coupled with impaired NK cell cytotoxicity and lower zinc ion than A- patients. However, the data reported are gender independent. Therefore, the -308A polymorphism at the locus of TNF-alpha may be one of the susceptibility factor for infectious diseases in old persons, particularly considering its association to the increased release of pro-inflammatory cytokines and to the reduction of zinc release and MTs synthesis involved in the control of the inflammatory response. These data strongly suggest that the genetic screening of the -308G/A polymorphism may be a valid tool for identification of subjects needing a more appropriate therapy when affected by acute and/or recurrent infectious diseases.
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PMID:The -308G/A polymorphism of TNF-alpha influences immunological parameters in old subjects affected by infectious diseases. 1568 88

Cinnamomum camphora Sieb (Lauraceae) has long been prescribed in traditional medicine for the treatment of inflammation-related diseases such as rheumatism, sprains, bronchitis and muscle pains. In this study, therefore, we aimed to investigate the inhibitory effects of Cinnamomum camphora on various inflammatory phenomena to explore its potential anti-inflammatory mechanisms under non-cytotoxic (less than 100 microg/ml) conditions. The total crude extract (100 microg/ml) prepared with 80% methanol (MeOH extract) and its fractions (100 microg/ml) obtained by solvent partition with hexane and ethyl acetate (EtOAc) significantly blocked the production of interleukin (IL)-1 beta, IL-6 and the tumor necrosis factor (TNF)-alpha from RAW264.7 cells stimulated by lipopolysaccharide (LPS) up to 20-70%. The hexane and EtOAc extracts (100 microg/ml) also inhibited nitric oxide (NO) production in LPS/interferon (IFN)-gamma-activated macrophages by 65%. The MeOH extract (100 microg/ml) as well as two fractions (100 microg/ml) prepared by solvent partition with n-butanol (BuOH) and EtOAc strongly suppressed the prostaglandin E(2) (PGE(2)) production in LPS/IFN-gamma-activated macrophages up to 70%. It is interesting to note that hexane, BuOH and EtOAc extracts (100 microg/ml) also inhibited the functional activation of beta1-integrins (CD29) assessed by U937 homotypic aggregation up to 70-80%. Furthermore, EtOAc and BuOH extracts displayed strong anti-oxidative activity with IC(50) values of 14 and 15 microM, respectively, when tested by the 1,1-diphenyl-2-picrylhydrazyl (DPPH) and xanthine oxide (XO) assays. Taken together, these data suggest that the anti-inflammatory actions of Cinnamomum camphora may be due to the modulation of cytokine, NO and PGE(2) production and oxidative stress, and of the subfractions tested, the EtOAc extract may be further studied to isolate the active anti-inflammatory principles.
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PMID:In vitro anti-inflammatory and anti-oxidative effects of Cinnamomum camphora extracts. 1618 79

Licorice, the roots of Glycyrrhiza inflata, is used by practitioners of alternative medicine to treat individuals with gastric or duodenal ulcers, bronchitis, cough, arthritis, adrenal insufficiency, and allergies. We investigated the anti-inflammatory properties of 4 licorice extracts: extracts of roasted licorice obtained by ethanol (rLE) or water extraction (rLW) and extracts of raw licorice obtained by ethanol (LE) or water extraction (LW). rLE demonstrated strong anti-inflammatory activity through its ability to reduce nitric oxide and prostaglandin E(2) production in the LPS-stimulated mouse macrophage cell, RAW264.7. It also inhibited the production of pro-inflammatory cytokines and CD14 expression on the LPS-stimulated RAW264.7 cells. Further study indicated that LPS-induced degradation and phosphorylation of Ikappa-Balpha, along with DNA-binding of NF-kappaB, was significantly inhibited by rLE exposure in RAW264.7 cells. In the murine model, we found that in vivo exposure to rLE-induced an increase in the survival rate, reduced plasma levels of TNF-alpha and IL-6, and increased IL-10 production in LPS-treated mice. Collectively, these data suggest that the use of rLE may be a useful therapeutic approach to various inflammatory diseases.
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PMID:Anti-inflammatory effect of roasted licorice extracts on lipopolysaccharide-induced inflammatory responses in murine macrophages. 1671 55

Viral infections in chickens pose a major health threat to the poultry industry. Infectious bronchitis virus (IBV) usually causes respiratory disease; however, the disease severity is influenced by the genotype of the chicken and the IBV strain involved. Nephropathogenic strains of IBV, such as the Australian T strain, can cause high mortalities due to kidney failure characterized by mononuclear cell infiltration and inflammation. In a previous study, a line of specific pathogen-free chickens, the S-line, was shown to be susceptible to high mortalities from IBV infection. The cause of these high mortalities is unknown but it is suspected that differential cytokine expression may play a role. With this in mind, we decided to study the role of the proinflammatory cytokine interleukin (IL)-6 during infection to determine its contribution to nephritis and influence on disease susceptibility. To investigate this, we infected the susceptible S-line and the more disease-resilient HWL line with the T strain of IBV and measured their cytokine response levels. In both lines of birds, IL-6 mRNA levels were elevated in the kidneys at 4 d postinfection. However, in S-line chickens, these levels were 20 times higher than those in the HWL chickens. In addition, S-line birds also showed three times higher serum IL-6 levels than HWL birds after IBV infection. These findings suggest that IL-6 may play a role in IBV-induced nephritis and may open an avenue to develop alternative strategies, such as the use of antiinflammatory cytokines, to overcome the nephropathogenic effects of IBV.
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PMID:Interleukin-6 expression after infectious bronchitis virus infection in chickens. 1793 Nov 18

In response to viral infection, the expression of numerous host genes, including predominantly a number of proinflammatory cytokines and chemokines, is usually up-regulated at both transcriptional and translational levels. It was noted that in cells infected with coronavirus, transcription and translation of some of these genes were differentially induced. Drastic induction of their expression at the transcriptional level was observed in cells infected with coronavirus. However, induction of the same genes at the translational level was usually found to be minimal to moderate. To investigate the underlying mechanisms, yeast two-hybrid screen was carried out using SARS-CoV proteins as baits, revealing that a subunit of the eukaryotic initiation factor 3 (eIF3), eIF3f, may interact with the N-terminal region of the SARS-CoV spike (S) protein. This interaction was subsequently confirmed by co-immunoprecipitation and immunofluorescent staining. Meanwhile, parallel experiments confirmed that eIF3f could also interact with the S protein of another coronavirus, the avian coronavirus infectious bronchitis virus (IBV). These interactions led to the inhibition of translation of a reporter gene in both in vitro expression system and intact cells. Interestingly, IBV-infected cells stably expressing a Flag-tagged eIF3f showed much higher translation of IL-6 and IL-8, suggesting that the interaction between coronavirus S protein and eIF3f plays a functional role in controlling the expression of host genes, especially genes that are induced during coronavirus infection cycles. This study reveals a novel mechanism exploited by coronavirus to regulate viral pathogenesis.
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PMID:Coronavirus spike protein inhibits host cell translation by interaction with eIF3f. 1823 81


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