Specific IgA against Pseudomonas aeruginosa in severe COPD

Laura Millares,1–3 Sara Martí,2,4 Carmen Ardanuy,2,4 Josefina Liñares,2,4 Salud Santos,2,5 Jordi Dorca,5 Marian García-Nuñez,1–3,6 Sara Quero,3,6 Eduard Monsó2,7,8 1Department of Respiratory Medicine, Fundació Parc Taulí, Sabadell, Spain; 2CIBER de Enfermedades Respiratorias, CIBERES, Bunyola, Spain; 3Universitat Autònoma de Barcelona, Esfera UAB, Barcelona, Spain; 4Department of Microbiology, Hospital Universitari de Bellvitge-Universitat de Barcelona-IDIBELL, L’Hospitalet de Llobregat, Spain; 5Department of Respiratory Medicine, Hospital Universitari de Bellvitge-Universitat de Barcelona-IDIBELL, L’Hospitalet de Llobregat, Spain; 6Infectious Diseases Unit, Fundació Insitut d’Investigació GermansTrias i Pujol, Badalona, Spain; 7Department of Respiratory Medicine, Hospital Universitari Parc Taulí, Sabadell, Spain; 8Department of Medicine, Universitat Autònoma de Barcelona (UAB), Barcelona, Spain 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 density450 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