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C Taube

Publications and source records attributed to C Taube.

At least 19 recordsLinked to original sources
PubMed2005

Strain-specific differences in perivascular inflammation in lungs in two murine models of allergic airway inflammation.

Histological data show perivascular recruitment of inflammatory cells in lung inflammation. However, the process of perivascular inflammation is yet-to-be characterized in any systematic manner at cell and molecular levels. Therefore, we investigated impact of genetic background on perivascular inflammation in acute or chronic airway inflammation in different strains of mice. Further, to address molecular mechanisms of perivascular inflammation, we examined immunohistochemical expression of vascular adhesion protein-1 (VAP-1) in chronic airway inflammation. Histological scoring revealed time and strain specific differences in perivascular recruitment of inflammatory cells in chronic and acute airway inflammation (P < 0.05). The data show that A/J strain is significantly more susceptible for perivascular inflammation followed by BALB/c and C57BL/6, while C3H/HeJ strain showed no perivascular accumulation of inflammatory cells. Of the two strains examined for perivascular inflammation in acute airway inflammation, BALB/c showed more accumulation of inflammatory cells compared to C57BL/c. VAP-1 expression occurred in the endothelium of pulmonary arteries but not in alveolar septa or airways in the control as well as challenged mice. In the inflamed lungs from A/J mice, the VAP-1 staining in pulmonary arteries was more intense compared to the other strains. VAP-1 staining was generally observed throughout the pulmonary arterial wall in chronic lung inflammation. These data show that periarterial inflammation is influenced by the genetic background, and may be partially regulated by VAP-1.

Acute Disease↗
PubMed2005

S-carboxymethylcysteine normalises airway responsiveness in sensitised and challenged mice.

S-carboxymethylcysteine (S-CMC) has been used as a mucoregulator in respiratory diseases. However, the mechanism of action of S-CMC on allergic airway inflammation has not yet been defined. In the present study, BALB/c mice were initially sensitised and challenged to ovalbumin (OVA) and, weeks later, re-challenged with OVA (secondary challenge). S-CMC (5-100 mg.kg-1) was administered from 2 days before the secondary challenge through to the day of assay. Mice developed airway hyperresponsiveness (AHR) 6 h after the secondary challenge and increased numbers of neutrophils were present in the bronchoalveolar lavage (BAL) fluid. At 72 h after secondary challenge, mice again developed AHR, but the BAL fluid contained large numbers of eosinophils. S-CMC treatment was found to reduce AHR and neutrophilia at 6 h, as well as eosinophilia and AHR at 72 h. These effects appeared to be dose dependent. Goblet cell hyperplasia, observed at 72 h, was reduced by S-CMC. In BAL fluid, increased levels of interferon-gamma, interleukin (IL)-12 and IL-10 and decreased levels of IL-5 and IL-13 were detected. In conclusion, the data indicate that S-carboxymethylcysteine is effective in reducing airway hyperresponsiveness and airway inflammation at two distinct phases of the response to the secondary allergen challenge in sensitised mice.

Allergens↗
PubMed2003

Reproducibility of forced inspiratory and expiratory volumes after bronchodilation in patients with COPD or asthma.

The aim of the present study was to assess the reproducibility of changes in forced inspiratory volumes after bronchodilator inhalation. Thirteen patients with chronic obstructive pulmonary disease (COPD) (FEV1, 32-75%pred) and 10 patients with asthma (FEV1, 43-75%pred) inhaled either 200 microg fenoterol or 200 microg oxitropium bromide or placebo, each of them on three occasions, on nine different days in a randomised, cross-over, double-blind fashion. Forced expiratory (FEV1) and inspiratory (FIV1) volumes were measured before and 30 min after inhalation. In patients with COPD, the increase in FEV1 (coefficient of variation) was 221 ml (43%) after fenoterol and 235 ml (33%) after oxitropium; changes in FIV1 were 301 ml (45%) and 360 ml (29%). In patients with asthma, FEV1 improved by 618 ml (26%) and 482 ml (25%), FIV1 by 553 ml (41%) and 475 ml (23%). In less severe COPD or asthma, the reduction in dyspnoea was associated with the improvements in both FIV1 and FEV1, but in severe COPD with the improvement in FIV1 only. The data demonstrate that, at least in terms of relative changes, the reproducibility of bronchodilator responses in terms of FIV1 is similar to that of FEV1 and they underline the assertion of FIV1 being a sensible parameter particularly in severe COPD.

Adrenergic beta-Agonists↗
PubMed2002

Pattern of NOS2 and NOS3 mRNA expression in human A549 cells and primary cultured AEC II.

The human alveolar type II epithelium-like cell line A549 expresses nitric oxide synthase type 2 (NOS2), but not NOS3, and produces nitric oxide (NO) upon appropriate stimulation. However, relatively little is known regarding the NOS2 and NOS3 expression of type II human alveolar epithelial cells (AEC II) in primary culture. We detected NOS3 mRNA in freshly isolated AEC II and after 24 h of culture. NOS3 mRNA levels were much higher in AEC II cultured for 24 h with or without interferon-gamma, interleukin-1beta, and tumor necrosis factor-alpha, compared with freshly isolated cells. Cytokine stimulation did not change the NOS3 mRNA expression level in AEC II compared with unstimulated cells. NOS3 protein expression was verified by Western blot, and measuring nitrate/nitrite revealed that the protein is active. In contrast, neither NOS2 mRNA nor protein could be detected in freshly isolated, unstimulated or cytokine-stimulated human AEC II in 24- or 72-h primary cultures, whereas A549 cells expressed NOS2 message and protein upon stimulation with proinflammatory cytokines. In situ hybridization confirmed that AEC II express NOS3, but not NOS2 mRNA in vivo. These data demonstrate that there are significant differences between primary AEC II and A549 cells in NOS mRNA expression pattern.

Adenocarcinoma↗
PubMed2002

Human alveolar epithelial cells induce nitric oxide synthase-2 expression in alveolar macrophages.

It was hypothesized that cell-to-cell interaction between human alveolar macrophages (AM) and alveolar epithelium, might be an important factor leading to nitric oxide synthase-2 (NOS2) messenger ribonucleic acid (mRNA) and protein expression by constituent cells of the alveolar wall and/or AM. NOS2 mRNA and the protein expression patterns of human AM and alveolar epithelial cells type II (AEC-II) isolated from normal parts of lung resections of patients with pulmonary malignancies were determined. In addition, NOS2 mRNA expression in human AM co-cultured with autologous AEC-II in the presence of pro-inflammatory cytokines interleukin (IL)-1beta, tumour necrosis factor (TNF)-alpha, interferon (IFN)-gamma or lipopolysaccharide (LPS) was investigated. The effect of human surfactant protein-A (SP-A) on IFN-gamma-mediated NOS2 mRNA expression in human AM was also studied. Neither NOS2 mRNA nor protein could be detected in freshly isolated, unstimulated or cytokine-stimulated AEC-II. In contrast, freshly isolated AM from bronchoalveolar lavage or lung tissue samples expressed immunoreactivity for NOS2 protein, but no NOS2 mRNA could be detected by reverse transcriptase polymerase chain reaction. All stimuli tested failed to induce NOS2 mRNA expression in human AM in vitro. Only AM-AEC-II co-culture in the presence of IFN-gamma led to NOS2 mRNA and protein expression. In situ hybridization of NOS2 mRNA on lung tissue explants and immunohistochemical staining of cytospin preparations of AM-AEC-II co-cultures demonstrated that NOS2 is expressed in AM but not in AEC-II. This co-culture effect could not be reproduced by substitution of AEC-II with SP-A. These data give evidence of a regulatory network controlling human nitric oxide synthase-2 expression in the lower respiratory tract.

Blotting, Western↗
PubMed2001

Airway response to inhaled hypertonic saline in patients with moderate to severe chronic obstructive pulmonary disease.

The present study aimed at delineating the mechanisms underlying the adverse response to hypertonic saline inhalation in patients with chronic obstructive pulmonary disease (COPD). Twenty patients (age, 48-70 yr; FEV(1), 29-58 %pred) inhaled, on two different days in randomized order, 200 microg salbutamol from an MDI and 20 min later either 0.9% or 3% saline from an ultrasonic nebulizer for a maximum of four consecutive 5-min periods. Forced expiratory (FEV(1)) and inspiratory (FIV(1)) volumes, inspiratory capacity (IC), intrathoracic gas volume (ITGV), and specific airway resistance (SRaw) were measured. Significant changes occurred in FEV(1), FIV(1), IC, ITGV, and SRaw with both concentrations (p < 0.05, each) and effects were stronger with 3% as compared with 0.9% saline (p < 0.05, each). The increase in dyspnea was associated with the changes in FIV(1), FEV(1), IC, and ITGV, in contrast to its decrease during bronchodilation, where only FIV(1) was important. Sputum analysis showed elevated concentrations of histamine after 3% as compared with 0.9% saline. These data indicate that the adverse lung function response to hypertonic saline is common in patients with moderate to severe COPD, involves both bronchoconstriction and lung hyperinflation, and could be mediated, at least partially, through activation of mast cells.

Administration, Inhalation↗
PubMed2001

In patients with chronic bronchitis a four week trial with inhaled steroids does not attenuate airway inflammation.

Systemic corticosteroids have been recommended as a therapeutic option in patients with moderate to severe COPD. In an early stage of the disease, i.e. chronic bronchitis with mild or no airflow obstruction, a trial with inhaled steroids could reveal potential benefits, particularly in terms of a modulation of airway inflammation. We therefore investigated the effect of inhaled fluticasone (1000 microg day(-1)) on markers of airway inflammation in 19 patients with chronic bronchitis (mean+/-SEM FEV1, 83.4+/-3.0% predicted; FEV1/VC, 67.5+/-2.4%) in a double-blind, cross-over, placebo-controlled manner. Visits were performed before and after two 4-week treatment periods. separated by a 4-week washout period. Lung function, the concentration of exhaled nitric oxide, differential cell counts in induced sputum and the number of cells positive for iNOS, as well as the levels of LDH, ECP, neutrophil elastase and IL-8 in sputum supernatants were determined. Although the total cell number decreased significantly after fluticasone (geometric mean 12.3 vs. 7.7 x 10(6)/ml; P<0.05) it was not significantly different from the change observed after placebo (14.2 vs. 10.6 x 10(6)/ml; n.s.). None of the other parameters showed statistically significant changes after fluticasone or placebo and the results did not depend on the presence of airway hyperresponsiveness. We conclude that in patients with chronic bronchitis short-term treatment with inhaled corticosterids did not improve lung function or inflammatory parameters to an extent which was statistically significant as compared to spontaneous variability.

Administration, Inhalation↗
PubMed2001

Nearly fatal complications of cervical lymphadenitis following BCG immunotherapy for superficial bladder cancer.

This report describes the case of a 68-year-old man with bilateral cervical lymphadenitis and chorioretinitis due to bacille Calmette-Guérin (BCG), originating from BCG immunotherapy for treatment of superficial bladder cancer 2 years ago. During antimycobacterial therapy a fistula between the right-sided lymph node and an aneurysm of the carotid artery developed. This led to life-threatening spontaneous bleeding which required vascular graft surgery. Like other known systemic side effects, cervical lymphadenitis may also occur following intravesical BCG immunotherapy, and life-threatening complications cannot be excluded despite adequate medical treatment.

Aged↗
PubMed2000

Home-based exercise is capable of preserving hospital-based improvements in severe chronic obstructive pulmonary disease.

We examined the feasibility of home-based walking training to maintain the benefits of a short-term exercise training in patients with severe chronic obstructive pulmonary disease (COPD). After initial recovery from an exacerbation, 46 patients were randomized into a training and a control group, and 30 patients completed the programme (mean +/- SD FEV1, 36 +/- 7% predicted). The training group performed a 10-day walking training programme in the hospital, followed by a 6-month programme of supervised walking training at home, integrated into daily activities. The control group did not have exercise training in the hospital or at home. Until 6 months after discharge, lung function, exercise performance and symptom scores were assessed. Six-minute walking distance in the training group improved from day 1 to day 10 (P<0.001) and this effect was maintained over 6 months (P<0.001). On average, daily walking distance at home was 2308 m and walking was reported on 157 days. Quality of life (QoL) scores changed significantly over 6 months (P<0.001). The control group showed no significant changes in exercise performance or QoL scores throughout the whole study period. Therefore, (i) significant improvements in exercise performance and Chronic Respiratory Disease Questionnaire (CRQ) scores could be achieved after recovery from an exacerbation and (ii) these improvements were maintained after discharge, when supported by a home-based walking training.

Aged↗
PubMed2000

Factor analysis of changes in dyspnea and lung function parameters after bronchodilation in chronic obstructive pulmonary disease.

Expiratory airway collapse is a characteristic feature in patients with chronic obstructive pulmonary disease (COPD). We hypothesized that this collapse might mask the effects of bronchodilators during forced expiration but not during forced inspiration, and that accordingly, the improvement in forced inspiration and not that in forced expiration with bronchodilator therapy would be related to changes in the perception of dyspnea. In order to investigate this, we conducted lung function measurements, including measurements of forced inspiration and expiration before and 30 min after inhalation of 400 microg salbutamol, in 61 patients with COPD (mean FEV(1): 38. 3 L; range: 12.9 to 79.5% predicted). The change in dyspnea from baseline was assessed with a standard visual analogue scale (VAS) ranging from -100 to +100. To delineate the relationship between parameters, we used the statistical procedure of factor analysis. Salbutamol induced an improvement of 0.16 +/- 0.02 L (mean +/- SD) in FEV(1), 0.36 +/- 0.04 L in forced inspiratory volume in one second (FIV(1)), 0.30 +/- 0.04 L in inspiratory capacity (IC), and -0.34 +/- 0.07 L in intrathoracic gas volume; the mean VAS score was 36.4 +/- 3.2. Factor analysis demonstrated that the reduction in dyspnea at rest was primarily associated with changes in parameters describing forced inspiration and not with those of forced expiration or lung hyperinflation, including IC. Our data indicate that in patients with COPD, the reduction in dyspnea after inhalation of a beta(2)-adrenoreceptor agonist is closely correlated with the change in parameters of forced inspiration, and particularly FIV(1), but not with changes in parameters of forced expiration or lung hyperinflation.

Albuterol↗
PubMed2000

Effect of proinflammatory cytokines on interleukin-8 mRNA expression and protein production by isolated human alveolar epithelial cells type II in primary culture.

Alveolar epithelial cells type II (AEC-II) are ideally situated to regulate the recruitment and activation of different types of cells through the production of chemokines in response to inflammatory stimulation from the alveolar space. We hypothesized that these cells are important producers of interleukin-8 (IL-8) in the lung. This lead us to investigate the capacity of isolated human AEC-II cells to release IL-8 and whether this IL-8 release is regulated by proinflammatory cytokines, i.e. IL-1 beta, TNF-alpha and IFN-gamma. We isolated AEC-II from tumor-free sections of human lungs obtained by pneumectomy and purified the cells by magnetic activated cell sorting. For control experiments the AEC-II-like cell line A549 was used. IL-8 concentration was measured by ELISA in supernatants of unstimulated and LPS-, IL-1 beta-, TNF-alpha- and IFN-gamma- stimulated cells. IL-8 mRNA expression was evaluated by RT-PCR. Spontaneous IL-8 mRNA expression and protein secretion by AEC-II were significantly higher in comparison with A549 cells. TNF-alpha increased both IL-8 mRNA expression and protein production, whereas IL-1 beta slightly increased IL-8 release but did not change mRNA expression in AEC-II. LPS and IFN-gamma did not influence IL-8 expression in AEC-II and A549 cells. These results show considerable differences between A549 cell and AEC-II. The latter are capable of producing IL-8 under the control of proinflammatory cytokines. Our findings demonstrate that the modulation of IL-8 release in AEC-II may have an important impact on the immunoreactivity of these cells during pulmonary inflammation in vivo.

Cells, Cultured↗
PubMed1998

Exercise training improves recovery in patients with COPD after an acute exacerbation.

Clinical experience suggests that exercise is beneficial for recovery after an acute exacerbation in patients with severe chronic obstructive pulmonary disease (COPD). The aim of this study was to quantify the clinical benefit of exercise in these patients. Twenty-nine inpatients were randomly assigned to a training group (n = 15, FEV1 34% pred) or a control group (n = 14, FEV1 38% pred). On ten consecutive days, patients in the training group performed a 6-min treadmill walking test and, in addition, five walking sessions per day at > or = 75% of the respective treadmill walking distance. Patients in the control group performed only treadmill walking tests on days 1, 5, and 10. To directly compare the possible benefit of exercise training all patients had an exercise test on day 11 at the same work load as on day 1. In the training group, 6-min walking distance increased from 237 to 420 m, in the control group from 230 to 255 m over the 10 day period which was significantly different (P < 0.0001). Minute ventilation and oxygen uptake increased significantly (P < 0.05) in the training but not in the control group. When comparing exercise tests on days 1 and 11, minute ventilation, oxygen uptake, PaCO2, lactic acid concentration, and Borg scale were significantly reduced to achieve the same work load (P < 0.01) only in the training group. Intrathoracic gas volume and residual volume decreased, and FEV1 and vital capacity increased in the training (P < 0.05) but not in the control group. Our data demonstrate that exercise training significantly improves the exercise capacity in patients with severe COPD after an acute exacerbation of their disease.

Aged↗
PubMed1998

Are chronic obstructive pulmonary disease (COPD) and asthma different diseases?

In the past it has been hypothesized that asthma and chronic obstructive pulmonary disease (COPD) are related diseases. As both show high prevalences and as smoking may occur in both groups of patients the simultaneous presence of both diseases in the same subject may well occur. The most characteristic features of asthma are short-term changes in airway caliber, reversible airflow limitation, bronchial hyperresponsiveness as well as eosinophilic and lymphocytic airway inflammation. The common definition of COPD implies long-term changes in airway calibre, less or irreversible airflow obstruction, no or less common bronchial hyperresponsiveness and neutrophilic airway inflammation. By analysing the results of epidemiology, risk factors, airway morphology, lung function and markers of airway inflammation in both diseases, it becomes clear that asthma and COPD share some similarities. However, their pathological presentations differ considerably and this provides evidence that the two syndromes are, in fact, different diseases. Furthermore, the analysis of data on lung volumes, diffusion capacity and aerosol-derived airway morphology shows important differences between asthma and COPD. It is suggested that the specific type of airway inflammation in both diseases is responsible for the peculiar pattern of lung function abnormalities.

Asthma↗
PubMed1993

U 46619 induces different blood pressure effects in male and female spontaneously hypertensive rats (SHR).

The effect of U 46619 (5 micrograms/kg i.v.) alone or in combination with acetylsalicylic acid (ASA) (100 mg/kg po.) on mean arterial blood pressure (MABP) was investigated in male and female spontaneously hypertensive rats (SHR). In male SHR, a significant increase of MABP was observed 1 min after administration of U 46619. Pretreatment of male SHR with ASA delayed the increase of MABP after intravenous injection of U 46619 compared to U 46619 alone. Whereas in control animals the elevated MABP returned to baseline values 5 min after intravenous application of U 46619, the MABP of ASA-pretreated male SHR remained significantly increased by about 30 mmHg. In contrast, the MABP of female SHR did not respond to U 46619 alone or to the combination of U 46619 and ASA. Sex differences were further shown by the vascular formation of thromboxane B2 (TXB2). Whereas in male SHR the vascular formation of TXB2 was increased by U 46619, the TXB2 formation of female SHR was decreased. The vascular formation of 6-keto-PGF1 alpha of male and female SHR was not influenced by U 46619 alone or a combination of U 46619 and ASA. In conclusion, our results demonstrate that the blood pressure of SHR respond differently to the TXA2 mimetic U 46619 in the two sexes. Furthermore, by modulating blood pressure response to TXA2, vasoactive prostanoids may be significantly involved in the maintenance of hypertension with male SHR.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Different effects of aspirin on blood pressure of spontaneously hypertensive rats (SHR) with high and spontaneously low levels of blood pressure.

Spontaneously hypertensive rats (SHR) of the Okamoto strain with blood pressure above 161 mmHg and SHR with blood pressure levels of less than 160 mmHg were treated with oral doses of aspirin (100 mg kg-1) for three days. Whereas the blood pressure of SHR with blood pressure above 161 mmHg was decreased by aspirin, the blood pressure of SHR below 160 mmHg was increased by aspirin. The extent and direction of blood pressure change by aspirin was strongly correlated with the blood pressure of SHR before treatment (r = -0.88). The effect of aspirin supports an important role for endogenous prostanoids in the regulation of blood pressure of SHR.

Animals↗
PubMed1992

Sexual dimorphism in blood pressure response to thromboxane agonist U 46619 and to endothelin.

The blood pressure rising effect of two vasconstrictoryacting substances (the thromboxan agonist U 46619 and the endothelium-derived peptide endothelin-1) differs in male and in female rats and this fact depends on normotensive or hypertensive levels of blood pressure. Whereas in male rats the drug effect was changed by pretreatment with aspirin, in female rats aspirin was uneffective in changing the blood pressure response to the agents. It could be suggested that the mechanism(s) for blood pressure regulation, especially the vasoconstrictor system, is different in males and females.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗