Study objective: To evaluate both the proliferation of
type II pneumocytes in the alveolitis associated with pulmonary
sarcoidosis and any alteration in their surface membrane antigenicity.
Materials and methods: We investigated 20
transbronchial lung biopsy (TBLB) specimens from 20 patients with
pulmonary sarcoidosis, 7 TBLB specimens from 7 sarcoidosis patients
without pulmonary involvement, and 19 normal lung specimens, using
colloidal iron stain and immunostaining with anti-Thomsen-Friedenreich
(TF) antigen and anti-surfactant protein-A monoclonal antibodies.
Results: The density of type II pneumocytes was
significantly higher in the pulmonary sarcoidosis specimens ([mean±
SD] 11.1 ± 3.7 per 1 mm alveolar septal length) than in the
nonpulmonary sarcoidosis (7.8 ± 1.3) or normal lung specimens
(7.2 ± 0.8). TF antigen was directly expressed on the apical surface
of some type II pneumocytes in the pulmonary sarcoidosis specimens, but
it was completely masked by sialic acids in the nonpulmonary
sarcoidosis specimens and in the normal lung tissues.
Conclusions: In pulmonary sarcoidosis, type II pneumocytes
proliferated and the antigenicity of the surface membrane was altered.
It is suggested that these type II pneumocytes may be vulnerable to
injury by natural anti-TF antibodies that are cytotoxic when present
with complement. This damage may decrease alveolar surfactant and cause
focal alveolar collapse proceeding to pulmonary fibrosis in some cases
of pulmonary sarcoidosis.