Smoking-induced inflammation of the airways associated with emphysema, in which the air sacs in the lungs are destroyed. The combination of chronic bronchitis and emphysema is known as chronic obstructive pulmonary disease. Symptoms include a productive cough and progressive breathlessness.
Chronic bronchitis is defined clinically as the presence of a chronic productive cough on most days for 3 months, in each of two consecutive years, in a patient in whom other causes of chronic cough have been excluded.
Chronic bronchitis can be classified into three forms:
- simple bronchitis, defined as mucus hypersecretion.
- chronic or recurrent mucopurulent bronchitis in the presence of persistent or intermittent mucopurulent sputum.
- chronic obstructive bronchitis when chronic sputum production is associated with airflow obstruction.
Cough and sputum production may precede the development of airflow limitation, but some patients develop airflow limitation without cough and sputum production.
The pathological basis of the hypersecretion of mucus in chronic bronchitis is an increase in the volume of the submucosal glands, and an increase in the number and a change in the distribution of goblet cells in the surface epithelium. Submucosal mucus glands are confined to the bronchi, decreasing in number and in size in the smaller, more peripheral bronchi, and not present in the bronchioles. In chronic bronchitis there is mucus gland hypertrophy in the larger bronchi with infiltration of the glands with inflammatory cells.
Above: The airway in a normal lung compared with one in chronic bronchitis
In healthy subjects who have never smoked, goblet cells are predominantly seen in the proximal airways and decrease in number in more distal airways, being absent normally in the terminal or respiratory bronchioles. By contrast, in smokers, goblet cells not only increase in number but extend more peripherally, hence mucus is produced in greater quantities in peripheral airways where the mucociliary escalator is less developed. Mucociliary function is also decreased in smokers. The use of bronchoscopy to obtain airway cells by bronchoalveolar lavage and bronchial tissue samples by biopsy has added new insights into the role of inflammation in COPD. Bronchial biopsy studies confirm those in resected lung tissue, which show bronchial wall inflammation in this condition see bullet points below:
Inflammation and inflammatory cells in COPD
- Neutrophils increase in sputum and distal air spaces in smokers, with a further increase in COPD related to disease severity. These are important in the secretion and release of proteases
- Macrophages increase in number in airways, lung parenchyma and in bronchoalveolar lavage fluid. These produce increased inflammatory mediators and proteases
- Eosinophils increase in airways walls, with increased eosinophil proteins in sputum, in some exacerbations of the disease.
As in asthma, bronchial biopsies in patients with chronic bronchitis reveal that activated T lymphocytes are prominent in the proximal airway walls. However, in contrast to asthma, macrophages also feature, and the CD8 suppressor T-lymphocyte subset (rather than CD4) predominates. Increased numbers of neutrophils are present, particularly in the glands, which become even more prominent as the disease progresses. Bronchial biopsies from limited studies in patients during exacerbations of chronic bronchitis show increased numbers of eosinophils in the bronchial walls, although their numbers are small compared with exacerbations of asthma and—unlike those in asthma—these cells do not appear to have degranulated. Bronchoalveolar lavage, or more recently studies of spontaneously produced or induced sputum, has shown increased intraluminal air space inflammation in patients with chronic bronchitis, with or without airways obstruction, with predominantly neutrophils and macrophages in the bronchoalveolar lavage studies. There is also evidence that air space inflammation in patients with chronic bronchitis persists following smoking cessation if the producti