T. Suzuki et al., 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-2 IN HUMAN LUNG - POSSIBLE REGULATOR OF MINERALOCORTICOID ACTION, The Journal of clinical endocrinology and metabolism, 83(11), 1998, pp. 4022-4025
11 beta-Hydroxysteroid dehydrogenase type 2 (11 beta HSD2) catalyzes t
he conversion of cortisol to biologically inactive cortisone and is th
ought to confer specificity on mineralocorticoid receptors (MR). Corti
sol is a prerequisite for surfactant synthesis and fetal lung maturati
on. Recently, expression of 11 beta HSD2 was demonstrated in human fet
al lung, but its localization and possible biological roles remain unk
nown. Therefore, in this study, we examined immunohistochemical locali
zation of 11 beta HSD2, MR, and glucocorticoid receptor (GR) in nonpat
hological human lungs from fetus to adult (8 weeks gestation to 55 yr
of age; n = 40) retrieved om pathology files. Both 11 beta HSD2 and MR
immunoreactivities were detected in airway epithelia, from bronchiole
to trachea and in fetal and neonatal ciliated collecting duct cells o
f tracheal and bronchial glands, but were undetectable in alveoli. On
the other hand, GR was detected in all cell types. These results indic
ate that 11 beta HSD2 colocalizes with MR in human airway epithelia an
d suggest that 11 beta HSD2 play an important role in pulmonary minera
locorticoid activity such as sodium and fluid transport.