Metabolic abnormalities exacerbate Sjögren’s syndrome by and is associated with increased the population of interleukin–17–producing cells in NOD/ShiLtJ mice

BACKGROUND: Sjögren’s syndrome (SS) is an autoimmune disease mediated by lymphocytic infiltration into exocrine glands, resulting in progressive lacrimal and salivary destruction and dysfunctional glandular secretion. Metabolic syndrome influences the immune system. To investigate its relationship with metabolic abnormalities, we evaluated the pathogenesis of SS and the immune cell populations in non-obese diabetic NOD/ShiLtJ mice with type 1 diabetes (T1D). METHODS: To induce metabolic abnormalities, streptozotocin (STZ)—a glucosamine–nitrosourea compound that destroys pancreatic β cells, resulting in T1D—was injected into NOD/ShiLtJ mice. The blood glucose level was measured to evaluate induction of T1D. The severity of SS was assessed by determining the body weight, salivary flow rate, and histologic parameters. The expression levels of proinflammatory factors in the salivary glands, lacrimal gland, and spleen were quantified by real–time PCR. The populations of various T– and B–cell subtypes in the peripheral blood, spleen, and salivary glands were assessed by flow cytometry. RESULTS: Induction of T1D in NOD/ShiLtJ mice increased both the severity of SS and the levels of proinflammatory cytokines in the salivary glands compared to the controls. Furthermore, the number of interleukin-17–producing immune cells in the peripheral blood, spleen, and salivary glands was increased in STZ- compared to vehicle-treated NOD/ShiLtJ mice. CONCLUSIONS: Metabolic abnormalities play an important role in the development of SS.