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)

A cytokine profile and changes in bone metabolism were studied in 95 patients (30 females and 65 males) with chronic obstructive pulmonary disease (COPD). Subnormal bone density was diagnosed in 78% patients with COPD. Frequency of osteoporosis discovery in emphysema was higher than in chronic obstructive bronchitis and the degree of density loss in bone tissue depended on ventilation disturbance. Intensification of bone resorption in relatively stable osteogenesis was encountered in 73.6% patients and manifested in elevated CrossLaps concentration. A close correlation exists between proinflammatory cytokines, bone density and indices of bone metabolism in COPD. This suggests a significant role of cytokine-mediated mechanisms in pathogenesis of pulmonogenic osteopenia.
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PMID:[Biochemical and immunological markers of osteoporosis in patients with chronic obstructive pulmonary disease]. 1247 35

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

Exposure to particulate matter (PM) may exacerbate preexisting respiratory diseases such as asthma, chronic obstructive pulmonary disease (COPD), bronchitis, and pneumonia. However, few experimental studies have addressed the effects of PM on lower respiratory tract (LRT) viral infection. Respiratory syncytial virus (RSV) is a major etiological agent for LRT infections in infants, the elderly, and the immunocompromised and may lead to chronic wheezing and the development of asthma in children. In this study, we examined the effects of carbon black (CB) on RSV-induced pulmonary inflammation, chemokine and cytokine expression, and airway hyperresponsiveness in a mouse model of RSV. Female BALB/c mice were instilled via the trachea (i.t.) with 1 x 106 plaque forming units (pfu) RSV or with uninfected culture media. On day 3 of infection, mice were i.t. instilled with either 40 micro g ultrafine CB particles or with saline. End points were examined on days 4, 5, 7, and 14 of RSV infection. Viral titer and clearance in the lung were unaffected by CB exposure. Neutrophil numbers were elevated on days 4 and 7, and lymphocyte numbers were higher on days 4 and 14 of infection in CB-exposed, RSV-infected mice. CB exposure also enhanced RSV-induced airway hyperresponsiveness to methacholine, bronchoalveolar lavage (BAL) total protein, and virus-associated chemokines monocyte chemoattractant protein (MCP-1), macrophage inflammatory protein (MIP-1 alpha), and regulated upon activation, normal T cell expressed and secreted (RANTES). MIP-1 alpha mRNA expression was increased in the alveolar epithelium, where ultrafine particles deposit in the lung. These data demonstrate a synergistic effect of ultrafine CB particles on RSV infection, and suggest a potential mechanism for increased respiratory infections in human populations after PM exposure.
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PMID:Ultrafine carbon black particles enhance respiratory syncytial virus-induced airway reactivity, pulmonary inflammation, and chemokine expression. 1265 33

Epidemiological studies have indicated that exposure to elevated levels of particulate matter exacerbates several pulmonary diseases, including asthma, bronchitis, and viral infections. Respiratory syncytial virus (RSV) is the major cause of bronchiolitis and pneumonia in infants and may lead to the development of asthma in childhood. To determine whether particle exposure modulates the immune response to RSV, eight-week-old female BALB/c mice received an intratracheal (i.t.) instillation of either 40 micro g ultrafine carbon black (CB) particles or vehicle. The following day, mice were i.t. instilled with either 106 pfu RSV or uninfected media. End points were examined 1, 2, 4, 7, and 10 days during RSV infection. Compared with RSV alone, tumor necrosis factor-alpha (TNF-alpha) protein was reduced in the bronchoalveolar lavage fluid (BALF) on days 1 and 2 of infection; there was also a reduction in BALF lymphocyte numbers on day 4, which correlated with reductions in both IFN-gamma-inducible protein (IP-10), lymphotactin, and IFN-gamma mRNAs in the lungs of RSV + CB mice. Multiprobe ribonuclease protection assays of RSV + CB lung tissue showed no changes in the RSV-associated chemokines regulated upon activation, normal T cell expressed and secreted (RANTES), eotaxin, monocyte chemoattractant protein (MCP-1), macrophage inflammatory protein (MIP)-1 alpha or MIP-1 beta. Viral titers in RSV + CB mice were lower than RSV on days 2-4 of infection. By day 7 of infection, however, neutrophil numbers, proinflammatory cytokine mRNA expression, and protein levels of TNF-alpha and the Th2 cytokine interleukin (IL)-13 were increased in the lungs of RSV + CB mice, indicating an exacerbation of infection. These data indicate that preexposure to ultrafine particles induces an inflammatory milieu promoting allergic immune responses rather than IFNgamma production necessary for microbial defense.
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PMID:Effect of preexposure to ultrafine carbon black on respiratory syncytial virus infection in mice. 1266 Mar 65

The recent understanding of the key role of adhesion molecules in the pathogenesis of chest allergy in parasitic infections may provide a pharmacological target for the associated asthmatic symptoms. Circulating levels of the endothelial cell adhesion molecules (CAMs): sICAM-1, sVCAM-1 and sE-selectin in sera of 18 allergic asthmatic patients. 16 fascioliasis cases (acute & chronic), 24 fascioliasis cases with allergic chest manifestations and 10 apparently healthy control subjects were estimated by ELISA method. Also, IL-4 serum level was evaluated in all groups. Chest allergy in association with fascioliasis included mainly bronchial asthma, beside eosinophilic bronchitis, persistent wheezing and chronic cough. The study provided evidence that adhesion molecules expression is up regulated in acute and chronic fascioliasis cases with allergic chest manifestations. sVCAM-1 seemed to be an early indicator of asthma development in human fascioliasis. IL-4 cytokine was suggested to be responsible for the increased expression especially in the chronic phase of the disease, yet the role of other cytokines cannot be excluded.
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PMID:Role of endothelial cell adhesion molecules in the development of allergy in human fascioliasis. 1273 9

A reactive ability of immunocompetent cells was assessed by the level of cytokines TNF alpha and IL-8 estimated by enzyme immunoassay ("Genzyme diagnostics" kit) in 18 patients with chronic obstructive bronchitis (mean age 58 +/- 4.2 years, mean duration of the disease 11.2 +/- 5.2 years) and 15 control patients matched for age, with normal external respiration function, free of chronic bronchopulmonary pathology and allergic diseases. The greatest differences in cytokine levels were registered between the control group and patients with moderate generalized irreversible obstruction. These patients had similar basal and E. coli LPS induced synthesis of the above cytokines showing the lack of cell reserves, adequate immune response to exogenic antigen.
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PMID:[Cytokine imbalance in patients with chronic obstructive bronchitis]. 1293 6

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

Chlamydia pneumoniae causes a range of respiratory infections including bronchitis, pharyngitis and pneumonia. Infection has also been implicated in exacerbation/initiation of asthma and chronic obstructive pulmonary disease (COPD) and may play a role in atherosclerosis and Alzheimer's disease. We have used a mouse model of Chlamydia respiratory infection to determine the effectiveness of intranasal (IN) and transcutaneous immunization (TCI) to prevent Chlamydia lung infection. Female BALB/c mice were immunized with chlamydial major outer membrane protein (MOMP) mixed with cholera toxin and CpG oligodeoxynucleotide adjuvants by either the IN or TCI routes. Serum and bronchoalveolar lavage (BAL) were collected for antibody analysis. Mononuclear cells from lung-draining lymph nodes were stimulated in vitro with MOMP and cytokine mRNA production determined by real time PCR. Animals were challenged with live Chlamydia and weighed daily following challenge. At day 10 (the peak of infection) animals were sacrificed and the numbers of recoverable Chlamydia in lungs determined by real time PCR. MOMP-specific antibody-secreting cells in lung tissues were also determined at day 10 post-infection. Both IN and TCI protected animals against weight loss compared to non-immunized controls with both immunized groups gaining weight by day 10-post challenge while controls had lost 6% of body weight. Both immunization protocols induced MOMP-specific IgG in serum and BAL while only IN immunization induced MOMP-specific IgA in BAL. Both immunization routes resulted in high numbers of MOMP-specific antibody-secreting cells in lung tissues (IN>TCI). Following in vitro re-stimulation of lung-draining lymph node cells with MOMP; IFNgamma mRNA increased 20-fold in cells from IN immunized animals (compared to non-immunized controls) while IFNgamma levels increased 6- to 7-fold in TCI animals. Ten days post challenge non-immunized animals had >7,000 IFU in their lungs, IN immunized animals <50 IFU and TCI immunized animals <1,500 IFU. Thus, both intranasal and transcutaneous immunization protected mice against respiratory challenge with Chlamydia. The best protection was obtained following IN immunization and correlated with IFNgamma production by mononuclear cells in lung-draining LN and MOMP-specific IgA in BAL.
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PMID:Comparison of intranasal and transcutaneous immunization for induction of protective immunity against Chlamydia muridarum respiratory tract infection. 1615 55

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

Extracts of Echinacea purpurea are among the most widely used herbal medicines throughout Europe and North America for the prevention or treatment of common cold, coughs, bronchitis and other upper respiratory infections. Popular preparations include expressed juice from the aerial parts of the plant (which contain polysaccharides) and alcoholic tinctures from roots (containing caffeic acid derivatives and alkylamides). Since immune modulation has been reported for similar extracts, cytokine antibody arrays were used to investigate the changes in the pro-inflammatory cytokines and chemokines released from a cultured line of human bronchial epithelial cells exposed to Rhinovirus 14 and two different chemically characterized Echinacea extracts. Virus infection stimulated the release of at least 31 cytokine-related molecules, including several important chemokines known to attract inflammatory cells. Most of these effects were reversed by simultaneous exposure to either of the two Echinacea extracts, although the patterns of response were different for the two extracts. These results could explain the antiinflammatory properties of Echinacea extracts. Furthermore, a number of these cytokines were stimulated by the same Echinacea preparations in uninfected cells. These observations therefore provide support for the alleged beneficial uses of Echinacea extracts.
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PMID:Echinacea extracts modulate the pattern of chemokine and cytokine secretion in rhinovirus-infected and uninfected epithelial cells. 1644 69


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