Abstract

Lymphocytic infiltration of the salivary glands in autoimmune diseases results in the human condition known as xerostomia. To date, an animal model for the autoimmune development of salivary gland dysfunction has yet to be described. With the autoimmune diabetes-prone nonobese diabetic (NOD) mouse strain, salivary flow rates and total saliva protein concentration in both male and female mice showed a progressive decline in the nondiabetic and diabetic states. Submandibular gland weight decreased from control mice with the progression to onset of diabetes in both sexes, whereas the weight of the parotid gland remained unchanged. The level of saliva amylase activity, when measured relative to unit volume, decreased in nondiabetic males but increased upon onset of diabetes to control values. When expressed relative to protein concentration in saliva, amylase activity was depressed for both sets of NOD mice but was higher upon diabetes onset than in the nondiabetic animals. In females a similar pattern was observed except that amylase activity expressed relative to unit volume was not significantly depressed in either set of NOD mice. The same observations were made for glandular amylase activity. The level of epidermal growth factor (a product of the ductal cells of the submandibular gland) was reduced over 500- and 18-fold for male and female diabetic mice, respectively. Sodium dodecyl sulfate polyacrylamide gels of total saliva showed changes in mobility as well as concentration of several proteins in the NOD mice.(ABSTRACT TRUNCATED AT 250 WORDS)

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