Ageing and smoking contribute to plasma surfactant proteins and protease imbalance with correlations to airway obstruction.

Background: A significant number of young people start smoking at an age of 13-15, which means that serious smoking-evoked changes may have been occurred by their twenties. Surfactant proteins (SP) and matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) have been linked to cigarette smoke induced lung remodelling and chronic obstructive pulmonary disease (COPD). However, the level of these proteins has not been examined during ageing or in young individuals with short smoking histories.

Matrix metalloproteinases -8, -9 and -12 in smokers and patients with stage 0 COPD.

COPD is underdiagnosed and its early assessment is problematic. It has been suggested that symptomatic smokers with normal FEV1/FVC (Stage 0 COPD, GOLD criteria) can develop COPD in the future. Potential early biomarkers in COPD include the matrix metalloproteinases (MMPs).

Transient elevation of neutrophil proteinases in induced sputum during COPD exacerbation.

Objective: Patients with chronic obstructive pulmonary disease (COPD) are prone to acute exacerbations associated with increased morbidity and mortality. One potential group of enzymes causing tissue destruction in this disease includes neutrophil proteinase elastase (NE), collagenase-2 (matrix metalloproteinase-8 (MMP-8)) and gelatinase B (MMP-9). We investigated the activity of NE and the levels of MMP-8 and MMP-9 in a longitudinal setting at and after COPD exacerbation using a non-invasive technique, i.

Increased oxidative stress in asymptomatic current chronic smokers and GOLD stage 0 COPD.

Background: Chronic obstructive pulmonary disease (COPD) is associated with increased oxidative and nitrosative stress. The aim of our study was to assess the importance of these factors in the airways of healthy smokers and symptomatic smokers without airway obstruction, i.e.