An inflammation in the bronchial wall is usually present already in an early stage of the disease. An inflammatory infiltration cause predominantly mononuclear cells in the mucous membrane and neutrophiles in the phlegm produced by airways. Also eosinophiles can participate in the inflammation. Lymphocytes distribution is different from asthma because there is mainly submucosa infiltrated in COPD. Metaplasia of goblet cells appears. Chronic bronchial obstruction characterizing COPD is induced by conjunction of small airways disease (obstructive bronchiolitis) and a destruction of pulmonary parenchyma (emphysema) which both contribute to an impairment and differ form person to person. Chronic inflammation is a cause of remodeling and narrowing of small airways. Destruction of pulmonary parenchyma and the inflammation cause loss of alveolar connection with small airways and elastic pulmonary stress decreases. Two theories try to explain COPD – a theory of imbalance between proteinases and antiproteinases and a theory of oxidation stress.

        Key words: Pathogenesis - Inflammation - Proteinases - Antiproteinases - Oxidation stress