Apoptosis and bcl-2 family expression in salivary gland from sjägrenös syndrome

Sjügrenös Syndrome (SS) is characterized by lymphocyte infiltrate in exocrine glands leading to destruction of glandular parenchyma resulting in xerostomia and xerophthalmia. In severe cases, SS salivary gland acini are destroyed and some ducts survive after an initial immune attack. To investigate the mechanism of acinar destruction and ductal survival, apoptosis and bcl-2, bax, bcl-x and bak expression were studied using in situ DNA nick end labeling and immunohistochemistry. SS salivary gland acinar and ductal epithelial cells (n-15) underwent apoptosis while normal salivary gland acinar cells (n-6) did not. Sites of high epithelial apoptosis showed the most structural abnormality based on &E staining. Few of the infiltrating mononuclear cells were apoptotic. A majority of infiltrating mononuclear cells in both SS and normal salivary gland strongly expressed bcl-2. However, bax, bcl-x and bak expression was either absent or weakly stained. Only a few of SS salivary ductal cells showed bcl-x+. Bak was not detected in both SS and normal salivary glands. Bcl-2 was expressed in SS ductal epithelial cells, but not in SS salivary gland acinar cells, normal ductal and acinar cells. SS salivary gland ductal and acinar cells were bax+t while normal acinar cells were not. Double staining for bax and apoptosis showed that the majority of bax+ acinar cells were apoptotic. SS salivary gland ductal cells co-expressed bcl-2 and bax. This suggests that an important mechanism of SS salivary gland destruction is apoptosis. Bax may be involved in cell death while bel-2 may protect SS ductal and infiltrating mononuclear cells from apoptosis.