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  • 1. Ahmadi, Zainab
    et al.
    Bornefalk-Hermansson, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Franklin, Karl A.
    Midgren, Bengt
    Ekstrom, Magnus P.
    Hypo- and hypercapnia predict mortality in oxygen-dependent chronic obstructive pulmonary disease: a population-based prospective study2014In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 15, p. 30-Article in journal (Refereed)
    Abstract [en]

    Background: The prognostic role of the arterial blood gas tension of carbon dioxide (PaCO2) in severe Chronic Obstructive Pulmonary Disease (COPD) remains unknown. The aim of this study was to estimate the association between PaCO2 and mortality in oxygen-dependent COPD. Methods: National prospective study of patients starting long-term oxygen therapy (LTOT) for COPD in Sweden between October 1, 2005 and June 30, 2009, with all-cause mortality as endpoint. The association between PaCO2 while breathing air, PaCO2 (air), and mortality was estimated using Cox regression adjusted for age, sex, arterial blood gas tension of oxygen (PaO2), World Health Organization performance status, body mass index, comorbidity, and medications. Results: Of 2,249 patients included, 1,129 (50%) died during a median 1.1 years (IQR 0.6-2.0 years) of observation. No patient was lost to follow-up. PaCO2 (air) independently predicted adjusted mortality (p < 0.001). The association with mortality was U-shaped, with the lowest mortality at approximately PaCO2 (air) 6.5 kPa and increased mortality at PaCO2 (air) below 5.0 kPa and above 7.0 kPa. Conclusion: In oxygen-dependent COPD, PaCO2 (air) is an independent prognostic factor with a U-shaped association with mortality.

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  • 2.
    Amin, Kawa
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Janson, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Sevéus, Lahja
    Miyazaki, Kaoru
    Virtanen, Ismo
    Venge, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Uncoordinated production of Laminin-5 chains in airways epithelium of allergic asthmatics2005In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 6, p. 110-Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Laminins are a group of proteins largely responsible for the anchorage of cells to basement membranes. We hypothesized that altered Laminin chain production in the bronchial mucosa might explain the phenomenon of epithelial cell shedding in asthma. The aim was to characterize the presence of Laminin chains in the SEBM and epithelium in allergic and non-allergic asthmatics.

    PATIENTS AND METHODS: Biopsies were taken from the bronchi of 11 patients with allergic and 9 patients with non-allergic asthma and from 7 controls and stained with antibodies against the Laminin (ln) chains alpha1-alpha5, beta1-beta2 and gamma1-gamma2.

    RESULTS: Lns-2,-5 and -10 were the main Laminins of SEBM. The layer of ln-10 was thicker in the two asthmatic groups while an increased thickness of lns-2 and -5 was only seen in allergic asthmatics. The ln gamma2-chain, which is only found in ln 5, was exclusively expressed in epithelial cells in association with epithelial injury and in the columnar epithelium of allergic asthmatics.

    CONCLUSION: The uncoordinated production of chains of ln-5 in allergic asthma could have a bearing on the poor epithelial cell anchorage in these patients.

  • 3.
    Andersson, Mikael
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Physiotheraphy. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Slinde, Frode
    Groenberg, Anne Marie
    Svantesson, Ulla
    Janson, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Emtner, Margareta
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Physiotheraphy. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Physical activity level and its clinical correlates in chronic obstructive pulmonary disease: a cross-sectional study2013In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 14, p. 128-Article in journal (Refereed)
    Abstract [en]

    Background: Decreased physical activity is associated with higher mortality in subjects with COPD. The aim of this study was to assess clinical characteristics and physical activity levels (PALs) in subjects with COPD. Methods: Seventy-three subjects with COPD (67 +/- 7 yrs, 44 female) with one-second forced expiratory volume percentage (FEV1%) predicted values of 43 +/- 16 were included. The ratio of total energy expenditure (TEE) and resting metabolic rate (RMR) was used to define the physical activity level (PAL) (PAL = TEE/RMR). TEE was assessed with an activity monitor (ActiReg), and RMR was measured by indirect calorimetry. Walking speed (measured over 30-meters), maximal quadriceps muscle strength, fat-free mass and systemic inflammation were measured as clinical characteristics. Hierarchical linear regression was applied to investigate the explanatory values of the clinical correlates to PAL. Results: The mean PAL was 1.47 +/- 0.19, and 92% of subjects were classified as physically very inactive or sedentary. The walking speed was 1.02 +/- 0.23 m/s, the quadriceps strength was 31.3 +/- 11.2 kg, and the fat-free mass index (FFMI) was 15.7 +/- 2.3 kg/m(2), identifying 42% of subjects as slow walkers, 21% as muscle-weak and 49% as FFM-depleted. The regression model explained 45.5% (p < 0.001) of the variance in PAL. The FEV1% predicted explained the largest proportion (22.5%), with further improvements in the model from walking speed (10.1%), muscle strength (7.0%) and FFMI (3.0%). Neither age, gender nor systemic inflammation contributed to the model. Conclusions: Apart from lung function, walking speed and muscle strength are important correlates of physical activity. Further explorations of the longitudinal effects of the factors characterizing the most inactive subjects are warranted.

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  • 4.
    Arnardóttir, Ragnheiður Harpa
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Emtner, Margareta
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Hedenström, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Larsson, Kjell
    Boman, Gunnar
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Peak exercise capacity estimated from incremental shuttle walking test in patients with COPD: A methodological study2006In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 7, p. 127-Article in journal (Refereed)
    Abstract [en]

    Background: In patients with COPD, both laboratory exercise tests and field walking tests are used to assess physical performance. In laboratory tests, peak exercise capacity in watts ( W peak) and/or peak oxygen uptake (VO2 peak) are assessed, whereas the performance on walking tests usually is expressed as distance walked. The aim of the study was to investigate the relationship between an incremental shuttle walking test (ISWT) and two laboratory cycle tests in order to assess whether W peak could be estimated from an ISWT.

    Methods: Ninety-three patients with moderate or severe COPD performed an ISWT, an incremental cycle test (ICT) to measure W peak and a semi-steady-state cycle test with breath-by-breath gas exchange analysis (CPET) to measure VO2 peak. Routine equations for conversion between cycle tests were used to estimate W peak from measured VO2 peak (CPET). Conversion equation for estimation of W peak from ISWT was found by univariate regression.

    Results: There was a significant correlation between W peak and distance walked on ISWT x body weight (r=0.88, p<0.0001). The agreement between W peak measured by ICT and estimated from ISWT was similar to the agreement between measured W peak (ICT) and W peak estimated from measured VO2 peak by CPET.

    Conclusion: Peak exercise capacity measured by an incremental cycle test could be estimated from an ISWT with similar accuracy as when estimated from peak oxygen uptake in patients with COPD.

  • 5. Eliason, Gabriella
    et al.
    Abdel-Halim, Samy M.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Piehl-Aulin, Karin
    Kadi, Fawzi
    Alterations in the muscle-to-capillary interface in patients with different degrees of chronic obstructive pulmonary disease2010In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 11, p. 97-Article in journal (Refereed)
    Abstract [en]

    Background: It is hypothesized that decreased capillarization of limb skeletal muscle is implicated in the decreased exercise tolerance in COPD patients. We have recently demonstrated decreased number of capillaries per muscle fibre (CAF) but no changes in CAF in relation to fibre area (CAFA), which is based on the diffusion distance between the capillary and muscle fibre. The aim of the current study is to investigate the muscle-to-capillary interface which is an important factor involved in oxygen supply to the muscle that has previously been suggested to be a more sensitive marker for changes in the capillary bed compared to CAF and CAFA. Methods: 23 COPD patients and 12 age-matched healthy subjects participated in the study. Muscle-to-capillary interface was assessed in muscle biopsies from the tibialis anterior muscle using the following parameters: 1) The capillary-to-fibre ratio (C:F-i) which is defined as the sum of the fractional contributions of all capillary contacts around the fibre 2) The ratio between C:F-i and the fibre perimeter (CFPE-index) 3) The ratio between length of capillary and fibre perimeter (LC/PF) which is also referred to as the index of tortuosity. Exercise capacity was determined using the 6-min walking test. Results: A positive correlation was found between CFPE-index and ascending disease severity with CFPE-index for type I fibres being significantly lower in patients with moderate and severe COPD. Furthermore, a positive correlation was observed between exercise capacity and CFPE-index for both type I and type IIa fibres. Conclusion: It can be concluded that the muscle-to-capillary interface is disturbed in the tibialis anterior muscle in patients with COPD and that interface is strongly correlated to increased disease severity and to decreased exercise capacity in this patient group.

  • 6. Franklin, Karl A
    et al.
    Janson, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Gíslason, Thórarinn
    Gulsvik, Amund
    Gunnbjörnsdottir, Maria
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Laerum, Birger N
    Lindberg, Eva
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Norrman, Eva
    Nyström, Lennarth
    Omenaas, Ernst
    Torén, Kjell
    Svanes, Cecilie
    Early life environment and snoring in adulthood2008In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 9, no 1, p. 63-Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: To our knowledge, no studies of the possible association of early life environment with snoring in adulthood have been published. We aimed to investigate whether early life environment is associated with snoring later in life. METHODS: A questionnaire including snoring frequency in adulthood and environmental factors in early life was obtained from 16,190 randomly selected men and women, aged 25-54 years, in Sweden, Norway, Iceland, Denmark and Estonia (response rate 74%). RESULTS: A total of 15,556 subjects answered the questions on snoring. Habitual snoring, defined as loud and disturbing snoring at least 3 nights a week, was reported by 18%. Being hospitalized for a respiratory infection before the age of two years (adjusted odds ratio (OR) = 1.27; 95% confidence interval (CI) 1.01-1.59), suffering from recurrent otitis as a child (OR = 1.18; 95%CI 1.05-1.33), growing up in a large family (OR = 1.04; 95%CI 1.002-1.07) and being exposed to a dog at home as a newborn (OR = 1.26; 95%CI 1.12-1.42) were independently related to snoring later in life and independent of a number of possible confounders in adulthood. The same childhood environmental factors except household size were also related with snoring and daytime sleepiness combined. CONCLUSION: The predisposition for adult snoring may be partly established early in life. Having had severe airway infections or recurrent otitis in childhood, being exposed to a dog as a newborn and growing up in a large family are environmental factors associated with snoring in adulthood.

  • 7. Gudmundsson, Gunnar
    et al.
    Gislason, Thorarinn
    Lindberg, Eva
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Hallin, Runa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Ulrik, Charlotte Suppli
    Bröndum, Eva
    Nieminen, Markku M.
    Aine, Tiina
    Bakke, Per
    Janson, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Mortality in COPD patients discharged from hospital: the role of treatment and co-morbidity2006In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 7, p. 109-Article in journal (Refereed)
    Abstract [en]

    Background: The aim of this study was to analyse mortality and associated risk factors, with special emphasis on health status, medications and co-morbidity, in patients with chronic obstructive pulmonary disease ( COPD) that had been hospitalized for acute exacerbation.

    Methods: This prospective study included 416 patients from each of the five Nordic countries that were followed for 24 months. The St. George's Respiratory Questionnaire (SGRQ) was administered. Information on treatment and co-morbidity was obtained.

    Results: During the follow-up 122 (29.3%) of the 416 patients died. Patients with diabetes had an increased mortality rate [HR = 2.25 (1.28 - 3.95)]. Other risk factors were advanced age, low FEV1 and lower health status. Patients treated with inhaled corticosteroids and/or long-acting beta-2-agonists had a lower risk of death than patients using neither of these types of treatment.

    Conclusion: Mortality was high after COPD admission, with older age, decreased lung function, lower health status and diabetes the most important risk factors. Treatment with inhaled corticosteroids and long-acting bronchodilators may be associated with lower mortality in patients with COPD.

  • 8. Ivanov, Stefan
    et al.
    Palmberg, Lena
    Venge, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Larsson, Kjell
    Lindén, Anders
    Interleukin-17A mRNA and protein expression within cells from the human bronchoalveolar space after exposure to organic dust2005In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 6, p. 44-Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: In mice, the cytokine interleukin (IL)-17A causes a local accumulation of neutrophils within the bronchoalveolar space. IL-17A may thereby also contribute to an increased local proteolytic burden. In the current study, we determined whether mRNA for IL-17A is elevated and protein expression of IL-17A occurs locally in inflammatory cells within the human bronchoalveolar space during severe inflammation caused by organic dust. We also assessed the expression of the elastinolytic protease MMP-9 in this airway compartment.

    METHODS: Six healthy, non-smoking human volunteers were exposed to organic dust in a swine confinement, a potent stimulus of neutrophil accumulation within the human bronchoalveolar space. Bronchoalveolar lavage (BAL) fluid was harvested 2 weeks before and 24 hours after the exposure and total and differential counts were conducted for inflammatory BAL cells. Messenger RNA for IL-17A was measured using reverse transcript polymerase chain reaction-enzyme linked immunoassay (RT-PCR-ELISA). Intracellular immunoreactivity (IR) for IL-17A and MMP-9, respectively, was determined in BAL cells.

    RESULTS: The exposure to organic dust caused more than a forty-fold increase of mRNA for IL-17A in BAL cells. IL-17A immunoreactivity was detected mainly in BAL lymphocytes, and the number of these IL-17A expressing lymphocytes displayed an eight-fold increase, even though not statistically significant. The increase in IL-17A mRNA was associated with a substantial increase of the number of BAL neutrophils expressing MMP-9 immunoreactivity.

    CONCLUSION: Exposure to organic dust increases local IL-17A mRNA and because there is intracellular expression in BAL lymphocytes, this suggests that IL-17A protein can originate from lymphocytes within the human bronchoalveolar space. The fact that the increased IL-17A mRNA is associated with an increased number of MMP-9-expressing neutrophils is compatible with IL-17A increasing the local proteolytic burden through its neutrophil-accumulating effect.

  • 9.
    Jonasson, Sofia
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Physiology.
    Swedin, Linda
    Lundqvist, Maria
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Physiology.
    Hedenstierna, Göran
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Dahlen, Sven-Erik
    Hjoberg, Josephine
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Physiology.
    Different effects of deep inspirations on central and peripheral airways in healthy and allergen-challenged mice2008In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 9, no 23Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Deep inspirations (DI) have bronchodilatory and bronchoprotective effects in healthy human subjects, but these effects appear to be absent in asthmatic lungs. We have characterized the effects of DI on lung mechanics during mechanical ventilation in healthy mice and in a murine model of acute and chronic airway inflammation. METHODS: Balb/c mice were sensitized to ovalbumin (OVA) and challenged with nebulized OVA for 1 week or 12 weeks. Control mice were challenged with PBS. Mice were randomly selected to receive DI, which was given twice during the minute before assessment of lung mechanics. RESULTS: DI protected against bronchoconstriction of central airways in healthy mice and in mice with acute airway inflammation, but not when OVA-induced chronic inflammation was present. DI reduced lung resistance induced by methacholine from 3.8+/-0.3 to 2.8+/-0.1 cmH2O*s*mL-1 in healthy mice and 5.1+/-0.3 to 3.5+/-0.3 cmH2O*s*mL-1 in acute airway inflammation (both P < 0.001). In healthy mice, DI reduced the maximum decrease in lung compliance from 15.9+/-1.5% to 5.6+/-0.6% (P < 0.0001). This protective effect was even more pronounced in mice with chronic inflammation where DI attenuated maximum decrease in compliance from 44.1+/-6.6% to 14.3+/-1.3% (P < 0.001). DI largely prevented increased peripheral tissue damping (G) and tissue elastance (H) in both healthy (G and H both P < 0.0001) and chronic allergen-treated animals (G and H both P < 0.0001). CONCLUSIONS: We have tested a mouse model of potential value for defining mechanisms and sites of action of DI in healthy and asthmatic human subjects. Our current results point to potent protective effects of DI on peripheral parts of chronically inflamed murine lungs and that presence of DI may blunt airway hyperreactivity.

  • 10. Kato, Bernet
    et al.
    Gulsvik, Amund
    Vollmer, William
    Janson, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Studnika, Michael
    Buist, Sonia
    Burney, Peter
    Can spirometric norms be set using pre- or post- bronchodilator test results in older people?2012In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 13, no 1, p. 102-Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    Chronic Obstructive Pulmonary Disease (COPD) is defined by post-bronchodilator spirometry. Data on "normal values" come predominantly from pre-bronchodilator spirometry. The effects of this on diagnosis are unknown.

    METHODS:

    Lower limits of normal (LLN) were estimated from "normal" participants in the Burden of Obstructive Lung Disease (BOLD) programme. Values separately derived using pre- and post-bronchodilator spirometry were compared. Sensitivity and specificity of criteria derived from pre-bronchodilator spirometry and pre-bronchodilator spirometry adjusted by a constant were assessed in the remaining population. The "gold standard" was the LLN for the post-bronchodilator spirometry in the "normal population". For FEV1/FVC, sensitivity and specificity of criteria were assessed when a fixed value of < 70% was used rather than LLN.

    RESULTS:

    Of 6,600 participants with full data, 1,354 were defined as "normal". Mean differences between pre- and post- bronchodilator measurements were small and the Bland-Altman plots showed no association between difference and mean value. Compared with using the gold standard, however, tests using pre-bronchodilator spirometry had a sensitivity and specificity of detecting a low FEV1 of 78.4% and 100%, a low FVC of 99.6% and 99.1% and a low FEV1/FVC ratio of 65% and 100%. Adjusting this by a constant improved the sensitivity without substantially altering the specificity for FEV1 (99%, 99.8%), FVC (97.4%, 99.9%) and FEV1/FVC (98.7%, 99.5%).

    CONCLUSIONS:

    Using pre-bronchodilator spirometry to derive norms for lung function reduces sensitivity compared to a post-bronchodilator gold standard. Adjustment of these values by a constant can improve validity of the test.

  • 11.
    Malinovschi, Andrei
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology.
    Janson, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Holmkvist, Thomas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology.
    Norbäck, Dan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Meriläinen, Pekka
    Högman, Marieann
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centre for Research and Development, Gävleborg.
    IgE sensitisation in relation to flow-independent nitric oxide exchange parameters2006In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 7, p. 92-Article in journal (Refereed)
    Abstract [en]

    Background: A positive association between IgE sensitisation and exhaled NO levels has been found in several studies, but there are no reports on the compartment of the lung that is responsible for the increase in exhaled NO levels seen in IgE-sensitised subjects.

    Methods: The present study comprised 288 adult subjects from the European Community Respiratory Health Survey II who were investigated in terms of lung function, IgE sensitisation ( sum of specific IgE), smoking history and presence of rhinitis and asthma. Mean airway tissue concentration of NO (Caw(NO)), airway transfer factor for NO (Daw(NO)), mean alveolar concentration of NO (Calv(NO)) and fractional exhaled concentration of NO at a flow rate of 50 mL s(-1) ( FENO0.05) were determined using the extended NO analysis.

    Results: IgE-sensitised subjects had higher levels ( geometric mean) of FENO 0.05 (24.9 vs. 17.3 ppb) ( p < 0.001), Daw(NO) ( 10.5 vs. 8 mL s(-1)) ( p = 0.02) and Caw(NO) (124 vs. 107 ppb) ( p < 0.001) and positive correlations were found between the sum of specific IgE and FENO 0.05, Caw(NO) and Daw(NO) levels ( p < 0.001 for all correlations). Sensitisation to cat allergen was the major determinant of exhaled NO when adjusting for type of sensitisation. Rhinitis and asthma were not associated with the increase in exhaled NO variables after adjusting for the degree of IgE sensitisation.

    Conclusion: The presence of IgE sensitisation and the degree of allergic sensitisation were related to the increase in airway NO transfer factor and the increase in NO concentration in the airway wall. Sensitisation to cat allergen was related to the highest increases in exhaled NO parameters. Our data suggest that exhaled NO is more a specific marker of allergic inflammation than a marker of asthma or rhinitis.

  • 12.
    Malinovschi, Andrei
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Physiology.
    Masoero, Monica
    Bellocchia, Michela
    Ciuffreda, Antonio
    Solidoro, Paolo
    Mattei, Alessio
    Mercante, Lorena
    Heffler, Enrico
    Rolla, Giovanni
    Bucca, Caterina
    Severe vitamin D deficiency is associated with frequent exacerbations and hospitalization in COPD patients2014In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 15, p. 131-Article in journal (Refereed)
    Abstract [en]

    Background: Acute exacerbations of COPD (AECOPD) are common and strongly influence disease severity and relative healthcare costs. Vitamin D deficiency is frequent among COPD patients and its contributory role in disease exacerbations is widely debated. Our aim was to assess the relationship of serum vitamin D levels with COPD severity and AECOPD. Methods: Serum vitamin D (25-hydroxyvitamin D) levels were measured in 97 COPD patients and related to lung function, comorbidities, FEV1 decline, AECOPD and hospital admission during the previous year. Results: Most patients (96%) had vitamin D deficiency, which was severe in 35 (36%). No significant relationship was found between vitamin D and FEV1 or annual FEV1 decline. No difference between patients with and without severe vitamin D deficiency was found in age, gender, BMI, smoking history, lung function, and comorbidities, apart from osteoporosis (60.9% in severe deficiency vs 22.7%, p = 0.001). In multiple logistic regression models, severe deficiency was independently associated with AECOPD [adjusted odds ratios (aOR) of 30.5 (95% CI 5.55, 168), p < 0.001] and hospitalization [aOR 3.83 (95% CI 1.29, 11.4), p = 0.02]. The odds ratio of being a frequent exacerbator if having severe vitamin D deficiency was 18.1 (95% CI 4.98, 65.8) (p < 0.001), while that of hospitalization was 4.57 (95% CI 1.83, 11.4) (p = 0.001). Conclusions: In COPD patients severe vitamin D deficiency was related to more frequent disease exacerbations and hospitalization during the year previous to the measurement of vitamin D. This association was independent of patients' characteristics and comorbidities.

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  • 13.
    Servetnyk, Zhanna
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
    Krjukova, Jelena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
    Gaston, Benjamin
    Zaman, Khalequz
    Hjelte, Lena
    Roomans, Godfried M.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
    Dragomir, Anca
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
    Activation of chloride transport in CF airway epithelial cell lines and primary CF nasal epithelial cells by S-nitrosoglutathione2006In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 7, p. 124-Article in journal (Refereed)
    Abstract [en]

    Background: It has been suggested that low mu M concentrations of S-nitrosoglutathione (GSNO), an endogenous bronchodilator, may promote maturation of the defective cystic fibrosis (CF) transmembrane conductance regulator ( CFTR). Because nitric oxide ( NO) and GSNO levels appear to be low in the CF airway, there is an interest in the possibility that GSNO replacement could be of therapeutic benefit in CF.

    Methods: The effect of GSNO on chloride (Cl-) transport was investigated in primary nasal epithelial cells obtained from CF patients homozygous for the delF508 mutation, as well as in two CF cell lines (CFBE and CFSME), using both a fluorescent Cl- indicator and X-ray microanalysis. Maturation of delF508 CFTR was determined by immunoblotting.

    Results: Treatment with 60 mu M GSNO for 4 hours increased cAMP-induced chloride efflux in nasal epithelial cells from 18 out of 21 CF patients, but did not significantly affect Cl- efflux in cells from healthy controls. This Cl- efflux was confirmed by measurements with a fluorescent Cl- indicator in the CFBE and CFSME cell lines. The effect of GSNO on Cl- efflux in CFBE cells could be inhibited both by a specific thiazolidinone CFTR inhibitor (CFTRinh-172) and by 4,4'-diisothiocyanatodihydrostilbene- 2,2'-disulfonic acid (H2DIDS). X-ray microanalysis showed that, following 4 hours incubation with 60 mu M GSNO, cAMP agonists caused a decrease in the cellular Cl- concentration in CFBE cells, corresponding to Cl- efflux. GSNO exposure resulted in an increase in the protein expression and maturation, as shown by immunoblot analysis. GSNO did not increase the cytosolic Ca2+ concentration in cultured airway epithelial cells.

    Conclusion: Previous studies have suggested that treatment with GSNO promotes maturation of delF508-CFTR, consistent with our results in this study. Here we show that GSNO increases chloride efflux, both in the two CF cell lines and in primary nasal epithelial cells from delF508-CF patients. This effect is at least in part mediated by CFTR. GSNO may be a candidate for pharmacological treatment of the defective chloride transport in CF epithelial cells.

  • 14. Smit, Lidwien A. M.
    et al.
    Kogevinas, Manolis
    Anto, Josep M.
    Bouzigon, Emmanuelle
    Ramon Gonzalez, Juan
    Le Moual, Nicole
    Kromhout, Hans
    Carsin, Anne-Elie
    Pin, Isabelle
    Jarvis, Deborah
    Vermeulen, Roel
    Janson, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Heinrich, Joachim
    Gut, Ivo
    Lathrop, Mark
    Valverde, Miguel A.
    Demenais, Florence
    Kauffmann, Francine
    Transient receptor potential genes, smoking, occupational exposures and cough in adults2012In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 13, p. 26-Article in journal (Refereed)
    Abstract [en]

    Background: Transient receptor potential (TRP) vanilloid and ankyrin cation channels are activated by various noxious chemicals and may play an important role in the pathogenesis of cough. The aim was to study the influence of single nucleotide polymorphisms (SNPs) in TRP genes and irritant exposures on cough.

    Methods: Nocturnal, usual, and chronic cough, smoking, and job history were obtained by questionnaire in 844 asthmatic and 2046 non-asthmatic adults from the Epidemiological study on the Genetics and Environment of Asthma (EGEA) and the European Community Respiratory Health Survey (ECRHS). Occupational exposures to vapors, gases, dusts, and/or fumes were assessed by a job-exposure matrix. Fifty-eight tagging SNPs in TRPV1, TRPV4, and TRPA1 were tested under an additive model.

    Results: Statistically significant associations of 6 TRPV1 SNPs with cough symptoms were found in non-asthmatics after correction for multiple comparisons. Results were consistent across the eight countries examined. Haplotype-based association analysis confirmed the single SNP analyses for nocturnal cough (7-SNP haplotype: p-global = 4.8 x 10(-6)) and usual cough (9-SNP haplotype: p-global = 4.5 x 10(-6)). Cough symptoms were associated with exposure to irritants such as cigarette smoke and occupational exposures (p < 0.05). Four polymorphisms in TRPV1 further increased the risk of cough symptoms from irritant exposures in asthmatics and non-asthmatics (interaction p < 0.05).

    Conclusions: TRPV1 SNPs were associated with cough among subjects without asthma from two independent studies in eight European countries. TRPV1 SNPs may enhance susceptibility to cough in current smokers and in subjects with a history of workplace exposures.

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  • 15.
    Ställberg, Björn
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Family Medicine and Clinical Epidemiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , Centrum för klinisk forskning i D län (CKFD).
    Selroos, Olof
    Vogelmeier, Claus
    Andersson, Eva
    Ekström, Tommy
    Larsson, Kjell
    Budesonide/formoterol as effective as prednisolone plus formoterol in acute exacerbations of COPD: a double-blind, randomised, non-inferiority, parallel-group, multicentre study2009In: Respiratory research (Online), ISSN 1465-9921, E-ISSN 1465-993X, Vol. 10, p. 11-Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Oral corticosteroids and inhaled bronchodilators with or without antibiotics represent standard treatment of COPD exacerbations of moderate severity. Frequent courses of oral steroids may be a safety issue. We wanted to evaluate in an out-patient setting whether a 2-week course of inhaled budesonide/formoterol would be equally effective for treatment of acute COPD exacerbations as standard therapy in patients judged by the investigator not to require hospitalisation. METHODS: This was a double-blind, randomised, non-inferiority, parallel-group, multicentre study comparing two treatment strategies; two weeks' treatment with inhaled budesonide/formoterol (320/9 microg, qid) was compared with prednisolone (30 mg once daily) plus inhaled formoterol (9 microg bid) in patients with acute exacerbations of COPD attending a primary health care centre. Inclusion criteria were progressive dyspnoea for less than one week, FEV1 30-60% of predicted normal after acute treatment with a single dose of oral corticosteroid plus nebulised salbutamol/ipratropium bromide and no requirement for subsequent immediate hospitalisation, i.e the clinical status after the acute treatment allowed for sending the patient home.A total of 109 patients (mean age 67 years, 33 pack-years, mean FEV1 45% of predicted) were randomized to two weeks' double-blind treatment with budesonide/formoterol or prednisolone plus formoterol and subsequent open-label budesonide/formoterol (320/9 microg bid) for another 12 weeks. Change in FEV1 was the primary efficacy variable. Non-inferiority was predefined. RESULTS: Non-inferiority of budesonide/formoterol was proven because the lower limit of FEV1-change (97.5% CI) was above 90% of the efficacy of the alternative treatment. Symptoms, quality of life, treatment failures, need for reliever medication (and exacerbations during follow-up) did not differ between the groups. No safety concerns were identified. CONCLUSION: High dose budesonide/formoterol was as effective as prednisolone plus formoterol for the ambulatory treatment of acute exacerbations in non-hospitalized COPD patients. An early increase in budesonide/formoterol dose may therefore be tried before oral corticosteroids are used. CLINICAL TRIAL REGISTRATION: NCT00259779.

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