Abstract
BackgroundSjögren’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).MethodsTo 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.ResultsInduction 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.ConclusionsMetabolic abnormalities play an important role in the development of SS.
Highlights
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
We investigated the role of metabolic abnormalities induced by streptozotocin (STZ)—a glucosamine–nitrosourea compound that destroys pancreatic β cells, resulting in a type 1 diabetes (T1D) phenotype [19] —in the pathogenesis of SS in non-obese diabetic (NOD)/ShiLtJ mice
Induction of T1D in NOD/ShiLtJ mice increases the severity of SS To evaluate the role of metabolic abnormalities in SS in vivo, 10-week-old female NOD/ShiLtJ mice were fasted for 24 h and STZ was administered intraperitoneally
Summary
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. 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). Sjögren’s syndrome (SS) is a systemic autoimmune disease characterized by infiltration of lymphocytes into the exocrine glands, inflammation, tissue damage, and dysfunctional glandular secretion. Destruction of the lacrimal and salivary glands, which typically occurs in patients with SS, results in ocular dryness. The non-obese diabetic (NOD) mouse is a widely used model for diabetes mellitus type 1, and recognized as an appropriate model to study autoimmune exocrinopathy prevalent in human SS patients. The subsequent tissue specific immunological attack, antibody directed against the cell surface muscarinic/cholinergic receptors appears and increased cytokines in salivary gland [5,6,7,8]
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