Pathophysiology of viral-induced exacerbations of COPD

Potena Alfredo¹, Caramori Gaetano², Casolari Paolo², Contoli Marco², Sebastian L Johnston³, Papi Alberto²

¹Unità Operativa di Fisiopatologia Respiratoria, Azienda Ospedaliera Universitaria Arcispedale S. Anna, Ferrara, Italy; ²Clinica Pneumologica, Università di Ferrara, Azienda Ospedaliera Universitaria Arcispedale S. Anna, Ferrara, Italy; ³Department of Respiratory Medicine, National Heart and Lung at Wright Fleming Institute of Infection and Immunity, Imperial College London, London, UK

Abstract: Inflammation of the lower airways is a central feature of chronic obstructive pulmonary disease (COPD). Inflammatory responses are associated with an increased expression of a cascade of proteins including cytokines, chemokines, growth factors, enzymes, adhesion molecules and receptors. In most cases the increased expression of these proteins is the result of enhanced gene transcription: many of these genes are not expressed in normal cells under resting conditions but they are induced in the inflammatory process in a cell-specific manner. Transcription factors regulate the expression of many pro-inflammatory genes and play a key role in the pathogenesis of airway inflammation. Many studies have suggested a role for viral infections as a causative agent of COPD exacerbations. In this review we will focus our attention on the relationship between common respiratory viral infections and the molecular and inflammatory mechanisms that lead to COPD exacerbation.