"Vicious cycle" theory of the pathogenesis of<unk> . The development of<unk>  requires two factors: an infectious insult and impaired drainage, obstruction, or a defect in host defense. This triggers a host immune response from neutrophils (elastases), reactive oxygen species, and inflammatory cytokines that results in progressive destruction of normal lung architecture. In particular, the elastic fibers of bronchi are affected. The result is permanent abnormal dilation and destruction of the major bronchi and bronchiole walls. The "vicious cycle" theory is the generally accepted explanation for the pathogenesis of<unk> . In this model, a predisposed individual develops an excessive inflammatory response to pulmonary infection or tissue injury. The inflammation that results is partially responsible for the structural damage to the airways. The structural abnormalities allow for the stasis of mucus, which favors continued chronic infection and the persistence of the vicious cycle. Endobronchial tuberculosis commonly leads to<unk> , either from bronchial stenosis or secondary traction from fibrosis. Traction<unk>  characteristically affects peripheral bronchi (which lack cartilage support) in areas of end-stage fibrosis.
Bronchiectasis
Chronic obstructive pulmonary disease
Plastic bronchitis
Tracheobronchomalacia
Bronchitis kettle
Asbestosis
Acute bronchitis
Dust pneumonia