Bronchopulmonary dysplasia (BPD), the most common cause of chronic lun
g disease in prematurely born infants, is histologically characterized
by various degrees of airway and alveolar septal fibrosis. Tryptase,
a serine protease specific to mast cells, has been shown to have poten
t fibroblast mitogenic properties and in addition has been shown to be
increased in adult fibrotic lung disorders. Based on this analogy, th
e distribution of pulmonary mast cells exhibiting tryptase immunoreact
ivity was investigated by immunoperoxidase staining in autopsy specime
ns of infants dying with BPD. Morphologically normal lung specimens fr
om similarly aged infants dying of sudden infant death syndrome (SIDS)
served as controls. Tryptase-positive mast cell counts were performed
at 250 x from at least 10 random fields in bronchial, peribronchiolar
, and alveolar regions. Compared to controls, in lung sections exhibit
ing typical histologic features of long-standing BPD, tryptase positiv
e cells were significantly increased in bronchial (23.9 +/- 3.6 vs 14.
4 +/- 2.3) and peribronchiolar (15.3 +/- 3.2 vs 4.63 +/- 0.6) regions
compared to controls (P < 0.05, Student's t test). In particular, alve
olar regions exhibiting moderate to severe degrees of septal fibrosis
exhibited a dramatic increase in the number of tryptase-positive cells
(9.83 +/- 1.89 vs 0.34 +/- 0.18, P = 0.003). These findings of a tryp
tase-positive mast cell hyperplasia in BPD suggest potential roles of
mast cells as well as tryptase in the pathogenesis of this disease. Pe
diatr Pulmonol, 1995; 19:336-343, (C) 1995 Wiley-Liss, inc.