Reduced sputum expression of interferon-stimulated genes in severe COPD

• Published in: International journal of chronic obstructive pulmonary disease Vol. 11; pp. 1485 - 1494
• Main Authors: Hilzendeger, Clarissa, da Silva, Jane, Henket, Monique, Schleich, Florence, Corhay, Jean Louis, Kebadze, Tatiana, Edwards, Michael R, Mallia, Patrick, Johnston, Sebastian L, Louis, Renaud
• Format: Journal Article Web Resource
• Language: English
• Published: New Zealand Dove Medical Press Ltd 01.01.2016; Dove Medical Press
• Subjects: 2',5'-Oligoadenylate Synthetase - genetics; 2',5'-Oligoadenylate Synthetase - immunology; Aged; Airway management; Bacterial infections; Belgium; Cardiovascular & respiratory systems; Case-Control Studies; Chronic obstructive pulmonary disease; COPD; Cross-Sectional Studies; Disease Progression; DNA, Viral - genetics; Enzymes; Female; Gene expression; Genetic Markers; Host-Pathogen Interactions; Human health sciences; Humans; Immunity, Innate - genetics; Infections; innate immunity; interferon-beta; Interferon-beta - genetics; Interferon-beta - immunology; interferon-lambda1; interferon-stimulated genes; Interferons; Interleukins - genetics; Interleukins - immunology; Male; Middle Aged; Myxovirus Resistance Proteins - genetics; Myxovirus Resistance Proteins - immunology; Original Research; Oxidoreductases Acting on CH-CH Group Donors; Picornaviridae - genetics; Picornaviridae - immunology; Picornaviridae Infections - diagnosis; Picornaviridae Infections - genetics; Picornaviridae Infections - immunology; Picornaviridae Infections - virology; Proteins - genetics; Proteins - immunology; Pulmonary Disease, Chronic Obstructive - diagnosis; Pulmonary Disease, Chronic Obstructive - genetics; Pulmonary Disease, Chronic Obstructive - immunology; Pulmonary Disease, Chronic Obstructive - virology; Reagents; Respiratory Tract Infections - diagnosis; Respiratory Tract Infections - genetics; Respiratory Tract Infections - immunology; Respiratory Tract Infections - virology; Sciences de la santé humaine; Sputum - chemistry; Sputum - immunology; Sputum - virology; Systèmes cardiovasculaire & respiratoire; Viral infections; Belgium; United States > US; Germany; interferon-stimulated genes; innate immunity; interferon-β; interferon-λ1; COPD
• ISSN: 1178-2005; 1176-9106; 1178-2005
• DOI: 10.2147/COPD.S105948

Exacerbations of COPD are frequent and commonly triggered by respiratory tract infections. The purpose of our study was to investigate innate immunity in stable COPD patients. Induced sputum was collected from 51 stable consecutive COPD patients recruited from the COPD Clinic of CHU Liege and 35 healthy subjects. Expression of interferons beta (IFN-β) and lambda1 (IL-29), IFN-stimulated genes (ISGs) MxA, OAS, and viperin were measured in total sputum cells by reverse transcription quantitative polymerase chain reaction (RT-qPCR). The presence of Picornaviruses was assessed by RT-PCR, while potential pathogenic microorganisms (PPM) were identified by sputum bacteriology. Expression of IL-29 was found in 16 of 51 COPD patients (31%) and in nine of 35 healthy subjects (26%), while IFN-β was detected in six of 51 COPD patients (12%) and in two of 35 healthy subjects (6%). ISGs were easily detectable in both groups. In the whole group of COPD patients, OAS expression was decreased (P<0.05), while that of viperin was increased (P<0.01) compared to healthy subjects. No difference was found with respect to MxA. COPD patients from group D of Global Initiative for Chronic Obstructive Lung Disease (GOLD) had reduced expression of all three ISGs (P<0.01 for MxA, P<0.05 for OAS, and P<0.01 for viperin) as compared to those of group B patients. Picornaviruses were detected in eight of 51 (16%) COPD patients vs four of 33 (12%) healthy subjects, while PPM were detected in seven of 39 (18%) COPD patients and associated with raised sputum neutrophil counts. IFN-β expression was raised when either picornavirus or PPM were detected (P=0.06), but no difference was seen regarding IL-29 or ISGs. ISGs expression was reduced in severe COPD that may favor exacerbation and contribute to disease progress by altering response to infection.