On low magnification, bronchiolocentric inflammation is identified by inflammation around small airways with or without reactive lymphoid hyperplasia, granulomas, or fibrosis (Figs. 7.1 and 7.2). A variety of insults involve the airways, including infections (especially bacterial and viral pneumonias), drug reactions, allo- and autoimmune lung injury, hypersensitivity pneumonitis, and inhalational injury. Inflammation can be primarily neutrophilic in bacterial infections (Fig. 7.3) or eosinophilic in drug reaction (Fig. 7.4). Various types of bronchiolitis are discussed in Chapter 39.

Inflammation of the bronchiole that progresses to mucosal denudation, fibrosis, and obliteration of the airway is termed constrictive bronchiolitis. Constrictive bronchiolitis surrounds, rather than fills, the lumen, resulting in extrinsic compression of the airway. It is most frequently related to inhalational injury, autoimmune connective tissue diseases, and alloimmune disease (termed “obliterative bronchiolitis” in allografts and “bronchiolitis obliterans syndrome” in bone marrow transplant patients). Histologically, the process progresses in phases from destructive bronchiolar inflammation, predominantly T-cell mediated, to peribronchiolar fibrosis with or without peribronchiolar metaplasia, followed by obliteration and scarring of bronchioles (Figs. 7.5, 7.6, 7.7). In the final phase, airways may be difficult to discern, having been replaced by nodules of scar and smooth muscle adjacent to the pulmonary artery branch.

Dilatation of the major airways, or bronchiectasis, is more common than distal dilatation (bronchiolectasis). There are two major pathways to bronchiectasis – inflammatory and noninflammatory. Chronic infections may damage the airway wall, usually at the level of the bronchus, resulting in a massively dilated structure (Fig. 7.8). Recurrent pneumonias in patients with cystic fibrosis make
them especially prone to the development of bronchiectasis (see Chapter 34).