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Specific IgA against Pseudomonas aeruginosa in severe COPD

BACKGROUND: 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...

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Autores principales: Millares, Laura, Martí, Sara, Ardanuy, Carmen, Liñares, Josefina, Santos, Salud, Dorca, Jordi, García-Nuñez, Marian, Quero, Sara, Monsó, Eduard
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5628678/
https://www.ncbi.nlm.nih.gov/pubmed/29033561
http://dx.doi.org/10.2147/COPD.S141701
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author Millares, Laura
Martí, Sara
Ardanuy, Carmen
Liñares, Josefina
Santos, Salud
Dorca, Jordi
García-Nuñez, Marian
Quero, Sara
Monsó, Eduard
author_facet Millares, Laura
Martí, Sara
Ardanuy, Carmen
Liñares, Josefina
Santos, Salud
Dorca, Jordi
García-Nuñez, Marian
Quero, Sara
Monsó, Eduard
author_sort Millares, Laura
collection PubMed
description BACKGROUND: 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. PURPOSE: The aim of this study was to determine IgA-mediated bronchial specific immune responses against Pseudomonas aeruginosa in stable patients with severe disease. METHODS: 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). RESULTS: 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. CONCLUSION: 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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spelling pubmed-56286782017-10-13 Specific IgA against Pseudomonas aeruginosa in severe COPD Millares, Laura Martí, Sara Ardanuy, Carmen Liñares, Josefina Santos, Salud Dorca, Jordi García-Nuñez, Marian Quero, Sara Monsó, Eduard Int J Chron Obstruct Pulmon Dis Original Research BACKGROUND: 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. PURPOSE: The aim of this study was to determine IgA-mediated bronchial specific immune responses against Pseudomonas aeruginosa in stable patients with severe disease. METHODS: 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). RESULTS: 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. CONCLUSION: 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. Dove Medical Press 2017-09-30 /pmc/articles/PMC5628678/ /pubmed/29033561 http://dx.doi.org/10.2147/COPD.S141701 Text en © 2017 Millares et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). 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.
spellingShingle Original Research
Millares, Laura
Martí, Sara
Ardanuy, Carmen
Liñares, Josefina
Santos, Salud
Dorca, Jordi
García-Nuñez, Marian
Quero, Sara
Monsó, Eduard
Specific IgA against Pseudomonas aeruginosa in severe COPD
title Specific IgA against Pseudomonas aeruginosa in severe COPD
title_full Specific IgA against Pseudomonas aeruginosa in severe COPD
title_fullStr Specific IgA against Pseudomonas aeruginosa in severe COPD
title_full_unstemmed Specific IgA against Pseudomonas aeruginosa in severe COPD
title_short Specific IgA against Pseudomonas aeruginosa in severe COPD
title_sort specific iga against pseudomonas aeruginosa in severe copd
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5628678/
https://www.ncbi.nlm.nih.gov/pubmed/29033561
http://dx.doi.org/10.2147/COPD.S141701
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