Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.

Cellular and Structural Changes

Inflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and lymphocytes. The airway epithelium undergoes squamous metaplasia, replacing ciliated cells with non-ciliated squamous cells, which impair mucociliary clearance and increase infection risk. Simultaneously, submucosal glands and goblet cells enlarge (hyperplasia and hypertrophy), producing excessive, thick mucus. This is reflected in an increased Reid index, with glands occupying over half the thickness of the bronchial wall. Mucus accumulation promotes bacterial colonization, recurrent infections, and ongoing airway damage.

Functional Consequences

Airway remodeling includes smooth muscle hypertrophy, fibrosis, and inflammatory thickening, narrowing airways—especially during expiration. Mucus plugs further obstruct bronchioles, causing airflow limitation, air trapping, and hyperinflation. This flattens the diaphragm, reduces tidal volume, and increases the work of breathing, sometimes producing a barrel-shaped chest.

Gas exchange is impaired due to ventilation–perfusion mismatch, where perfusion exceeds ventilation, leading to hypoxemia and, in advanced cases, hypercapnia due to poor carbon dioxide clearance.

Clinical Impact

These changes result in chronic productive cough, dyspnea, and frequent infections. Although lung parenchyma is relatively preserved compared to emphysema, progressive airway damage leads to declining lung function.