Chronic obstructive pulmonary disease (COPD) has now become a global epidemic, affects over 300 million individuals world-wide, has become the third most common cause of death and is one of the leading causes of chronic morbidity and hospitalization, resulting in an enormous economic burden.This special issue of Chronic Obstructive Pulmonary Diseases: Journal of the COPD Foundation includes 3 important new analyses of the large COPD Genetic Epidemiology (COPDGene®) cohort concerning diagnosis, progression and the consequences of this disease.These striking new data have important implications for how we should define COPD in the future and how we should recognize different phenotypes.This will also be important in directing a search for new disease-modifying therapies that Editorial: The Pressing Need to Redefine COPD
Potentially pathogenic micro-organisms (PPMs) are frequently isolated from stable COPD patients. We hypothesised that the degree of airway & systemic inflammation is dependent on species of PPM. Sputa & sera collected from stable patients in the London COPD Cohort were analysed by qPCR to detect H. influenzae (HI) , M. catarrhalis (MC) and S. pneumoniae (SP), ELISAs for airway IL-8, IL-1β & MPO, & sera CRP was measured. 183 paired sputa & sera from 99 stable patients were included. Clinical characteristics are shown in Table 1. View this table: Baseline Characteristics n=99 PPMs were detected in 64/183 of sputa. HI & SP were equally prevalent & there was no significant difference between their loads (p=0.49). MC load was significantly higher than both HI (p<0.001) & SP (p=0.001). Patients with lower airway bacterial colonisation (LABC) by any PPM had significantly higher airway cytokines than non-LABC patients (all p<0.001). HI-colonised but not SP- or MC-colonised patients had significantly higher airway cytokines than non-LABC patients (all p<0.05, Figure 1). There was no significant difference between CRP in non-LABC & LABC patients, or between non-LABC patients & different PPMs. ![Figure][1] LABC patients have higher airway, but not systemic inflammation, & this is associated with HI. Targeting HI in stable COPD may potentially help to decrease airway inflammation. [1]: pending:yes