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      Specific IgA against Pseudomonas aeruginosa in severe COPD

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          The bronchial mucosa is protected by a specialized immune system focused on the prevention of colonization and infection by potentially pathogenic microorganisms (PPMs). Immunoglobulin A (IgA) is the principal antibody involved in this mechanism. A defective immune barrier may facilitate the recurrent presence of PPMs in COPD.


          The aim of this study was to determine IgA-mediated bronchial specific immune responses against Pseudomonas aeruginosa in stable patients with severe disease.


          COPD patients with good-quality sputum samples obtained during stability were included and classified according to the presence or absence of chronic bronchial colonization by P. aeruginosa. Levels of specific IgA for P. aeruginosa in sputum were determined by ELISA and expressed as ratios, using the pooled level of 10 healthy subjects as reference (optical density 450 patient/control).


          Thirty-six stable COPD patients were included, 15 of whom had chronic colonization by P. aeruginosa. Levels of specific IgA against P. aeruginosa in stable non-colonized patients were lower than those in healthy subjects (IgA ratio: median =0.15 [interquartile range {IQR} 0.05–0.36]). Colonized patients had higher levels, (1.56 [IQR 0.59–2.79]) ( p<0.001, Mann–Whitney U test), with figures equivalent but not exceeding the reference value.


          IgA-based immune response against P. aeruginosa was low in severe COPD patients. Levels of specific IgA against this microorganism were higher in colonized patients, but did not attain clear-cut levels above the reference. An impaired local response against P. aeruginosa may favor chronic colonization and recurrent infections in severe COPD.

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          Most cited references 13

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          Microscopic and baceriologic analysis of expectorated sputum.

          Samples of expectorated sputum were examined grossly and microscopically to determine their suitability for bacterial cultures. Microscopically, specimens were categorized according to the number of leukocytes and squamous epithelial cells (SEC) observed under low-power (times 100) in a Gram-stained smear. The mean number of species isolated was greater than 4 from specimens with more than 10 SEC per field, 2.7 from specimens with fewer than 10 SEC per field, and 2.4 from transtracheal aspirates. Oropharyngeal flora was isolated from nearly all of the specimens with more than 10 SEC per field, and potential pathogens were found in less than 15% of such specimens. The bacterial flora of specimens with fewer than 10 SEC per field closely resembled that of transtracheal aspirates.
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            Spirometric reference values from a Mediterranean population.

            Maximal expiratory flow-volume (MEFV) curves were measured in 1044 healthy nonsmoking volunteers living in the Barcelona area, as part of a larger interhospital project to obtain reference values of pulmonary function tests. Forced vital capacity (FVC), one-second forced expiratory volume (FEV1), FEV1/FVC, %, forced maximal mid-expiratory flow (FEF25-75%), peak expiratory flow rate (PEF) and maximal expiratory flow at 50 and 75% of FVC (MEF50% and MEF25% respectively) were obtained and expressed at BTPS conditions. Techniques and equipments followed both the recommendations of the American Thoracic Society (ATS) and of the European Community for Coal and Steel (ECCS). Prediction equations for age 20 through 70 were calculated for both sexes from a final sample composed of 870 adult subjects, 443 males and 427 females. Simple linear equations using height, age and body weight predicted all spirometric variables as well as more complex equations except MEF25%. Logarithmic equations were proposed for MEF25% to correct for the heteroscedasticity shown in a simple linear model. To our knowledge, this study provides reliable spirometric equations from a large urban Mediterranean sample which were lacking so far in the literature.
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              Bronchial secretory immunoglobulin a deficiency correlates with airway inflammation and progression of chronic obstructive pulmonary disease.

              Although airway inflammation can persist for years after smoking cessation in patients with chronic obstructive pulmonary disease (COPD), the mechanisms of persistent inflammation are largely unknown. We investigated relationships between bronchial epithelial remodeling, polymeric immunoglobulin receptor (pIgR) expression, secretory IgA (SIgA), airway inflammation, and mural remodeling in COPD. Lung tissue specimens and bronchoalveolar lavage were obtained from lifetime nonsmokers and former smokers with or without COPD. Epithelial structural changes were quantified by morphometric analysis. Expression of pIgR was determined by immunostaining and real-time polymerase chain reaction. Immunohistochemistry was performed for IgA, CD4 and CD8 lymphocytes, and cytomegalovirus and Epstein-Barr virus antigens. Total IgA and SIgA were measured by ELISA and IgA transcytosis was studied using cultured human bronchial epithelial cells. Areas of bronchial mucosa covered by normal pseudostratified ciliated epithelium were characterized by pIgR expression with SIgA present on the mucosal surface. In contrast, areas of bronchial epithelial remodeling had reduced pIgR expression, localized SIgA deficiency, and increased CD4(+) and CD8(+) lymphocyte infiltration. In small airways (<2 mm), these changes were associated with presence of herpesvirus antigens, airway wall remodeling, and airflow limitation in patients with COPD. Patients with COPD had reduced SIgA in bronchoalveolar lavage. Air-liquid interface epithelial cell cultures revealed that complete epithelial differentiation was required for normal pIgR expression and IgA transcytosis. Our findings indicate that epithelial structural abnormalities lead to localized SIgA deficiency in COPD airways. Impaired mucosal immunity may contribute to persistent airway inflammation and progressive airway remodeling in COPD.

                Author and article information

                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                30 September 2017
                : 12
                : 2807-2811
                [1 ]Department of Respiratory Medicine, Fundació Parc Taulí, Sabadell, Spain
                [2 ]CIBER de Enfermedades Respiratorias, CIBERES, Bunyola, Spain
                [3 ]Universitat Autònoma de Barcelona, Esfera UAB, Barcelona, Spain
                [4 ]Department of Microbiology, Hospital Universitari de Bellvitge-Universitat de Barcelona-IDIBELL, L’Hospitalet de Llobregat, Spain
                [5 ]Department of Respiratory Medicine, Hospital Universitari de Bellvitge-Universitat de Barcelona-IDIBELL, L’Hospitalet de Llobregat, Spain
                [6 ]Infectious Diseases Unit, Fundació Insitut d’Investigació GermansTrias i Pujol, Badalona, Spain
                [7 ]Department of Respiratory Medicine, Hospital Universitari Parc Taulí, Sabadell, Spain
                [8 ]Department of Medicine, Universitat Autònoma de Barcelona (UAB), Barcelona, Spain
                Author notes
                Correspondence: Eduard Monsó, Hospital Universitari Parc Taulí, Parc Taulí 1, 08208 Sabadell, Barcelona, Spain, Tel +34 937 23 10 10 ext 29115, Fax +34 937 45 84 53, Email emonso@
                © 2017 Millares et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Original Research

                Respiratory medicine

                immunoglobulin a, sputum, copd, colonization, elisa


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