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Laboratory and Animal Investigations |

Proliferation of Type II Pneumocytes and Alteration in Their Apical Surface Membrane Antigenicity in Pulmonary Sarcoidosis*

Muneharu Hayasaka, MD; Takayuki Honda, MD; Keishi Kubo, MD; Morie Sekiguchi, MD
Author and Funding Information

*From the Department of Internal Medicine (Drs. Hayasaka, Kubo, and Sekiguchi) and the Department of Laboratory Medicine (Dr. Honda), Shinshu University School of Medicine, Matsumoto, Japan.

Correspondence to: Takayuki Honda, MD, Department of Laboratory Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, 390-8621 Japan; e-mail: thondat@hsp.md.shinshu-u.ac.jp



Chest. 1999;116(2):477-483. doi:10.1378/chest.116.2.477
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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.

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